Hepatocellular carcinoma (HCC) is the most common primary liver cancer and a leading cause of cancer mortality worldwide. Its pathogenesis reflects a combination of tumour-intrinsic heterogeneity and a profoundly immunosuppressive tumour microenvironment. Growing evidence shows that tumours recapitulate developmental programs to establish an oncofetal ecosystem, characterised by the re-expression of foetal antigens and foetal-like stromal and immune subsets. These features drive immune evasion and shape therapeutic response, contributing to immunotherapy outcomes in clinic. This review outlines mechanistic insights into oncofetal reprogramming across tumour, stromal, and immune compartments and evaluates therapeutic strategies that target these dependencies. We highlight emerging vaccine platforms, cellular therapies, and biologics targeting oncofetal antigens, with particular emphasis on mRNA–lipid nanoparticle vaccines and their potential to induce robust, durable antitumour immunity. We further discuss rational combinatorial strategies that integrate vaccines with immune checkpoint inhibitors. Finally, we discuss how overcoming liver tolerance and antigenic heterogeneity will be essential for effective oncofetal-directed therapies. Collectively, targeting the oncofetal ecosystem through coordinated vaccine, cellular, and immunotherapeutic strategies offers a path toward more durable responses and broader immunotherapy benefits in HCC.

Background: Nitrous oxide has been an integral part of surgical anesthesia for many years in the developed world and is still used in developing countries such as India. The other main concerns in low-resource countries are the lack of an advanced anesthesia gas-scavenging system and modular surgical theatres. As a greenhouse gas that has been present in the atmosphere for more than 100 years and damages the ozone layer, nitrous oxide is three times worse than sevoflurane. Here, we conducted an observational study to quantify the annual nitrous oxide consumption and its environmental impact in terms of carbon dioxide equivalence in one of busiest tertiary health care and research centers in Northern India. Methods: Data related to nitrous oxide expenditure’ from the operation theatre and manifold complex of our tertiary care hospital and research center from 2018 to 2021 were collected monthly and analyzed. The outcomes were extracted from our observational study, which was approved by our institutional ethics board (INT/IEC/2017/1372 Dated 25.11.2017) and registered prospectively under the Central Registry (CTRI/2018/07/014745 Dated 05.07.2018). Results: The annual nitrous oxide consumption in our tertiary care hospital was 22,081.00, 22,904.00, 17,456.00, and 18,392.00 m 3 (cubic meters) in 2018, 2019, 2020, and 2021, respectively. This indicates that the environmental impact of nitrous oxide (in terms of CO2 equivalents) from our hospital in 2018, 2019, 2020, and 2021 was 13,016.64, 13,287.82, 10,289.94, and 10,841.24 tons, respectively. Conclusion This huge amount of nitrous oxide splurge is no longer a matter of laughter, and serious efforts should be made at every central and peripheral health center level to reduce it.

Background/Aims: Intestinal tuberculosis (ITB) is difficult to diagnose due to poor sensitivity of definitive diagnostic tests. ITB may be associated with concomitant pulmonary tuberculosis (PTB) which may remain undetected on chest X-ray. We assessed the role of contrast enhanced computed tomography (CECT) chest in detecting the prevalence of active PTB, and increasing the diagnostic yield in patients with suspected ITB. Methods: Consecutive treatment naïve patients with suspected ITB (n=200) who underwent CECT chest (n=88) and had follow-up duration>1 year were recruited in this retrospective study (February 2016 to October 2018). ITB was diagnosed in the presence of caseating granuloma, positive acid fast stain or culture for Mycobacterium tuberculosis on biopsy, presence of necrotic lymph nodes (LNs) on CT enterography or positive response to anti-tubercular therapy. Evidence of active tuberculosis on CECT-chest was defined as presence of centrilobular nodules with or without consolidation/miliary nodules/thick-walled cavity/enlarged necrotic mediastinal LNs. Results: Sixty-five of eighty-eight patients (mean age, 33.8±12.8 years; 47.7% of females) were finally diagnosed as ITB (4-caseating granuloma on biopsy, 12-necrotic LNs on CT enterography, 1-both, and 48-response to anti-tubercular therapy) and 23 were diagnosed as Crohn’s disease. Findings of active TB on CECT chest with or without necrotic abdominal LNs were demonstrated in 5 and 20 patients, respectively. No patient with Crohn’s disease had necrotic abdominal LNs or active PTB. Addition of CECT chest in the diagnostic algorithm improved the sensitivity of ITB diagnosis from 26.2% to 56.9%. Conclusions Addition of CECT chest significantly improves the sensitivity for definite diagnosis in a patient with suspected ITB.

Methods: Amplitude and latency of TcMEPs were recorded bilaterally from the abductor pollicis brevis (APB) and abductor hallucis (AH) muscles in 38 adult American Society of Anesthesiologists I and II patients undergoing thoracolumbar spine surgery. Baseline recordings of TcMEPs in both groups were recorded under propofol infusion. Group X patients then received propofol and fentanyl (1 mcg/kg/hr), and group Y patients received ketofol and fentanyl (1 mcg/kg/hr). Bispectral index was maintained at 40–60 in both groups. Amplitude and latency were recorded at 30 minutes intervals for 2 hours. Results: Propofol caused no significant changes in amplitude and latency in any muscle. In contrast, amplitude increased significantly at all time points in the bilateral APB muscles and 60, 90, and 120 minutes in the left AH muscle without changes in latency in response to ketofol. When the two groups were compared, ketofol induced significantly higher amplitudes at 60, 90, and 120 minutes in the (left) APB, at all time points in the (right) APB, and at 120 minutes in both AH muscles, compared with propofol. Blood pressures were lower and fluid and vasopressor requirements were higher in group X. Muscle power was similar between the two groups. Conclusions Ketofol facilitates TcMEP amplitudes without affecting latency. Use of ketofol resulted in a better and more stable hemodynamic profile than did use of propofol.

Background/Aims: Liver cirrhosis is an important cause of morbidity and mortality globally. Every episode of decompensation and hospitalization reduces survival. We studied the clinical profile and long-term outcomes comparing alcohol-related cirrhosis (ALC) and non-ALC.
Methods: Cirrhosis patients at index hospitalisation (from January 2010 to June 2017), with ≥1 year follow-up were included.
Results: Five thousand and one hundred thirty-eight cirrhosis patients (age, 49.8±14.6 years; male, 79.5%; alcohol, 39.5%; Child-A:B:C, 11.7%:41.6%:46.8%) from their index hospitalization were analysed. The median time from diagnosis of cirrhosis to index hospitalization was 2 years (0.2–10). One thousand and seven hundred seven patients (33.2%) died within a year; 1,248 (24.3%) during index hospitalization. 59.5% (2,316/3,890) of the survivors, required at least one readmission, with additional mortality of 19.8% (459/2,316). ALC compared to non-ALC were more often (P<0.001) male (97.7% vs. 67.7%), younger (40–50 group, 36.2% vs. 20.2%; P<0.001) with higher liver related complications at baseline, (P<0.001 for each), sepsis: 20.3% vs. 14.9%; ascites: 82.2% vs. 65.9%; spontaneous bacterial peritonitis: 21.8% vs. 15.7%; hepatic encephalopathy: 41.0% vs. 25.0%; acute variceal bleeding: 32.0% vs. 23.7%; and acute kidney injury 30.5% vs. 19.6%. ALC patients had higher Child-Pugh (10.6±2.0 vs. 9.0±2.3), model for end-stage liver-disease scores (21.49±8.47 vs. 16.85±7.79), and higher mortality (42.3% vs. 27.3%, P<0.001) compared to non-ALC.
Conclusions One-third of cirrhosis patients die in index hospitalization. 60% of the survivors require at least one rehospitalization within a year. ALC patients present with higher morbidity and mortality and at a younger age.

Carotid body tumor excision can lead to various complications including vascular injury and pseudoaneurysm formation. Here we describe a case of carotid body tumor excision followed by series of complications including pseudoaneurysm formation, failure of primary surgical repair, carotid stump syndrome following parent artery occlusion, and persistent hypotension.