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Rewired metabolism is a hallmark of pancreatic ductal adenocarcinomas (PDA). Previously, we demonstrated that PDA cells enhance glycosylation precursor biogenesis through the hexosamine biosynthetic pathway (HBP) via activation of the rate limiting enzyme, glutamine-fructose 6-phosphate amidotransferase 1 (GFAT1). Here, we genetically ablated GFAT1 in human PDA cell lines, which completely blocked proliferation in vitro and led to cell death. In contrast, GFAT1 knockout did not preclude the growth of human tumor xenografts in mice, suggesting that cancer cells can maintain fidelity of glycosylation precursor pools by scavenging nutrients from the tumor microenvironment. We found that hyaluronic acid (HA), an abundant carbohydrate polymer in pancreatic tumors composed of repeating N -acetyl-glucosamine (GlcNAc) and glucuronic acid sugars, can bypass GFAT1 to refuel the HBP via the GlcNAc salvage pathway. Together, these data show HA can serve as a nutrient fueling PDA metabolism beyond its previously appreciated structural and signaling roles.

We present a case of narrow complex, near simultaneous “A on V” tachycardia in a patient with diseased His bundle (intrahisian delay:35 ms; HV: 72 ms) and describe response to adenosine, RV overdrive pacing and parahisian resetting to elucidate the tachycardia mechanism.

Exposure to high levels of air pollution and extreme heat stress has been individually linked to significant health and economic problems in India. However, not much is known about the threats resulting from the co-occurrence of these hazards, which have common meteorological drivers. In this study, we perform a country-wide joint risk analysis at the district level, examining the risks of chronic exposure to the joint extremes of particulate matter (PM 2.5 ) pollution (PM 2.5 , mass of particles smaller than 2.5 µ m in diameter) and heat stress (wet bulb globe temperature) in the presence of geophysical and socioeconomic vulnerability. We find that northern, central, and eastern India are at alarming levels of joint risk, potentially exposing 61% (∼842 million) of the population and 56% (∼1.84 million km²) of land area. Spatially differentiated drivers of joint risk are high levels of PM 2.5 in northern India, high heat hazards in northern and eastern India, and high vulnerability in the central and eastern states of Chhattisgarh, Madhya Pradesh, Bihar, West Bengal, and Odisha. Region-specific response actions for long-term risk mitigation include reducing emissions from residential and agricultural biomass combustion and industrial coal-burning sources, as well as addressing the challenges of housing, healthcare delivery, and economic conditions in central and eastern India. A coordinated policy framework aimed at tackling individual hazards is vital to alleviating these joint risks.

The case highlights the possibility of nonischemic cardiomyopathy in patients with coronary artery disease and the complex nature of the isthmus with multiple entry and exit points. A combination of multiple strategies, that is, unipolar mapping, isochronal late activation mapping during sinus rhythm, and positioning of a multielectrode catheter at the putative isthmus during VT induction in the case of hemodynamically unstable VT, was used to achieve a successful outcome.

The fourth universal definition of MI defines requires presence of j point elevation in two contiguous leads except v2–3 where the elevation should be equal to or >2 mm in men (2.5 mm in <40 years) and 1.5 mm in women.(1) We present two cases of patients who presented with electrocardiographic manifestations of occlusion of septal perforator of left anterior descending artery and discuss the salient feature of ECG in such patients. We also present the limitations of STEMI criteria given the dynamic nature of acute coronary occlusion and stress on early recognition of this MI.

Continuous anthropogenic inputs have raised environmental concerns regarding non-degradable plastics derived from non-renewable petrochemicals, creating an urgent need for sustainable alternatives and driving a paradigm shift toward bioplastics. This review investigates the transformative role of the natural biopolymer xanthan gum as an eco-friendly additive in advancing biodegradable materials. Derived from Xanthomonas campestris, xanthan gum offers non-toxicity, biodegradability, and strong compatibility. The literature indicates that its negative charge enables interactions with positively charged molecules, enhancing composite properties such as mechanical strength. Although xanthan gum has limitations when used alone, it functions as an effective additive in packaging applications. The novelty of this work lies in exploring diverse techniques and formulations for integrating xanthan gum into bioplastic films and coatings, emphasizing its role in reinforcing biopolymer structures. As a sustainable alternative, xanthan gum-based composites preserve food quality and extend shelf life by providing protection against moisture, oxygen, UV radiation, and microbial contamination. Realizing its full potential requires optimized formulations to prevent structural disruptions and reduced stretchability at higher xanthan gum concentrations. Continued research, especially leveraging nanotechnology, is essential to amplify its advantages and address related challenges. This review highlights xanthan gum’s pivotal contribution to bioplastic innovation, presenting a strong case for its broader adoption in the food packaging industry.

Both transient elastography (TE)-based and non-TE-based criteria exist for detection of varices needing treatment (VNT) in patients with asymptomatic advanced chronic liver disease (CLD). However, their performance in clinical settings at different risk thresholds of detection of VNT and in regions where elastography is not widely available is unknown. We aimed to validate existing noninvasive criteria in our patients with CLD and identify best TE- and non-TE-based criteria for VNT screening at usual risk thresholds. Patients with compensated advanced CLD (cACLD) who underwent esophagogastroduodenoscopy and TE within 3 months were included. Diagnostic performance of Baveno VI, expanded Baveno VI, platelet-model for end-stage liver disease, and platelet-albumin (Rete Sicilia Selezione Terapia-hepatitis C virus) criteria were estimated. Decision curve analysis was conducted for different predictors across range of threshold probabilities. A repeat analysis including all patients with compensated CLD (cACLD and non-cACLD) was performed to simulate absence of TE. A total of 1,657 patients (cACLD, 895; non-cACLD, 762) related to hepatitis B virus (38.2%), hepatitis C virus (33.4%), nonalcoholic steatohepatitis (14.7%), and alcohol (11.8%) were included. Baveno VI identified maximum VNT (97.3%) and had best negative predictive value (96.9%), followed by platelet-albumin criteria. Expanded Baveno VI and platelet-model for end-stage liver disease had intermediate performance. At threshold probability of 5%, Baveno VI criteria showed maximum net benefit, and platelet-albumin criteria was next best, with need for 95 additional elastographies to detect 1 additional VNT. Similar results were obtained on including all patients with compensated CLD irrespective of TE. Baveno VI criteria maximizes VNT yield at 5% threshold probability. An acceptable alternative is the platelet-albumin criteria in resource-limited settings.

The cardiac causes predominantly include rheumatic heart disease, mitral valve prolapse and congenital heart disease. Since the patient presented in junctional rhythm, our main differential included either transient causes (new onset atrial fibrillation, transient electrolyte abnormalities (hyperkalaemia), digoxin toxicity, acute myocarditis with atrial involvement, dilated cardiomyopathy) or permanent causes (associated with muscular dystrophies and genetic cardiomyopathies). Atrial standstill is a rare condition with absence of atrial mechanical/electrical activity characterized by “(1) the absence of P waves in the ECG and of A waves in the intracardiac recordings, (2) narrow QRS complexes, (3) evidence of atrial paralysis (absence of A waves in the jugular venous pulse, in the atrial pressure recording and in the mitral Doppler recording), and (4) inability to stimulate the atria.” Germline pathogenic variations in the HCN4 gene have been shown to be associated with familial sick sinus syndrome, specifically the autosomal dominant type 2 variety.5 The mechanism by which sick sinus syndrome due to gene mutations result in atrial standstill have been best described for SCN5A mutation which is the most common genetic cause in paediatric patients with atrial standstill.1 In patients with SCN5A mutations, slowing down of both pacemaker function and conduction of action potential across the SA node-atrium occurs.6 Histological examination of the atrial wall have been described to show presence of dense collagenous tissue, different stages of fibrosis with scattered myocardium.7 A combination of reducing pacemaking activity and atrial fibrosis contributes to the atrial standstill.