Ascariasis remains a major burden of disease globally, with an estimated prevalence of 1 billion individuals being affected. Previous studies have highlighted a strong association and geographical overlap between worm infestation and TB infection. In these same studies, the occurrence of helminth-tuberculosis coinfection has been described and is postulated to be a result of immune modulation induced by both etiological organisms. An 81 year old male with history of laparoscopic cholecystectomy presented with acute pancreatitis and cholangitis. An abdominal Ultrasound was performed which excluded biliary dilatation and evidence of gall stones. Nevertheless, in view of a high index of suspicion of biliary obstruction, we proceeded with an Endoscopic Ultrasound (EUS) procedure which revealed multiple long, tubular, hyperechoic structures with an anechoic centre that spanned the entire length of the Common Bile Duct. The echogenic structures did not exhibit posterior acoustic shadowing and appeared mobile which was in keeping with biliary ascariasis. In addition, multiple large matted lymph nodes were observed at the periportal, hilar and -peripancreatic region. EUS-FNB of the biopsied hilar lymph node was in keeping with reactive lymphadenitis. Endoscopic Retrograde Cholangiopancreatography (ERCP) was subsequently performed and multiple linear imbricated, bile coated structures which was in keeping with macerated worms were trawled out from the CBD. Patient was given Albendazole therapy and repeat endoscopic evaluation revealed eradication of Ascariasis.

This review is done to briefly highlight the therapeutic options available for NAFLD (Non-Alcoholic Fatty Liver Disease), and the role of anti-oxidants in support of NAFLD. PubMed and Google Scholar search was done using the keywords such as NAFLD, Liver cirrhosis, fibrosis, steatosis, anti-oxidants, inflammatory markers, apoptosis. This review article contains precise data from a few crucial recent articles that throw light on the current situation and treatment options available for NAFLD patients. NAFLD was recently re-termed as MAFLD (Metabolic Associated fatty Liver Disease) and has started affecting a significant proportion of the population mainly due to the incidence of metabolic syndrome as one of the greatest risk factors of NAFLD. Therapeutic options for the same have been studied for a long time but no single effective option has been discovered yet. Understanding the mechanism of NAFLD has led to the use of vitamins especially vitamin E and other substances such as polyphenols which are the emerging new options included for the treatment. These targets the reactive oxygen species, inflammatory markers, modulate fatty acid oxidation, and insulin resistance. Recent guidelines have recommended the use of Vitamin E in biopsy-proven NAFLD patients without diabetes. On the contrary, vitamin E has side effects seen at certain doses due to which the therapeutic ability although most effective, is limited in such patients. Despite the risk profile, vitamin E is still considered one of the safest options due to patient tolerability and improvement in NAFLD stages that has been proven histologically as well but in non-diabetic patients. This article also provides a brief insight into other therapeutic options available in the category of nutrients. There is a need for research to look into more options available as treatment and also to identify the risk and benefits of vitamin E to find a more permanent therapeutic solution for NAFLD patients.

In recent years, clinical and animal studies have confirmed that metabolic associated fatty liver disease (MAFLD) is a multisystem disease. The extrahepatic complications of MAFLD, including cardiovascular disease, tumors, metabolic nephropathy, obstructive apnea syndrome, osteoporosis, psoriasis, iron overload, and various metabolic and endocrine diseases, are closely related. The incidence of these diseases is far higher than that of the liver disease itself. This article provides a comprehensive review of the correlation between MAFLD and psoriasis. Studies have shown that MAFLD is a common disease in adult patients with psoriasis. MAFLD is associated with a higher likelihood of developing metabolic syndrome and more severe skin disease in patients with psoriasis. In addition, patients with psoriasis are more likely to develop more severe MAFLD. However, further research is needed to clarify the biological mechanisms of MAFLD and psoriasis. Healthcare providers of patients with psoriasis should watch for the development of this liver disease. The coexistence of MAFLD should also be considered when planning treatment, because of the potential hepatotoxic effects of some conventional drugs for the treatment of psoriasis.

We report this unusual case of a one-day-old infant who presented with hematemesis and was found to have congenital duodenal web, The Diagnosis was made by Upper GI Imaging and Endoscopy and management was done by surgical repair. Congenital duodenal obstruction carries a risk of duodenitis in newborns, and they may present with acute hematemesis. The management includes early surgery to relieve the obstruction.

To assess clinicopathological characteristics of gastrointestinal stromal tumor (GIST) and the relationship between tumor necrosis factors and patient prognosis.

Data of 60 patients with gastric cancer (GC) admitted from September 2018 to April 2019 at the Hunan Provincial People's Hospital were collected. Clinicopathological characteristics were analyzed to assess the correlation between tumor necrosis factor and clinicopathological characteristics, immunohistochemical expression, and prognosis.

A difference was noted between tumor necrosis and tumor size, nucleosis imaging, NIH risk grade, and desmin in GC patients (P < 0.05), and between tumor necrosis and sex, age, site, and levels and immunohistochemical index of DOG-1, CD117, CD34, and SMA (P > 0.05).

There is a correlation between tumor necrosis and tumor size, nuclear division image, NIH risk grade, and desmin, and patients with GC have tumor necrosis and patient prognosis.

The leading cause of dementia is Alzheimer’s disease (AD), which affects millions worldwide. Aging populations can foretell the worsening burden of the disease in the future. AD is characterised by the following hallmark pathologies: amyloid-β over-production and deposition, abnormal hyperphosphorylation of tau leading to the formation of neurofibrillary tangles, and neuroinflammation. Many potential treatments fail in clinical trials, suggesting that present theories are outdated or lead to therapeutic dead-ends. A gum disease-causing species of bacteria, Porphyromonas gingivalis, is being increasingly linked with AD, given the ubiquity of gum disease amongst older populations, and studies have revealed that the bacteria causes and exacerbates AD pathology both in vitro and in vivo. P. gingivalis produce many neurotoxic molecules, including gingipain enzymes, lipopolysaccharide and phosphoglycerol dihydroceramides, and all of these have been shown to affect AD pathologies. Numerous mechanisms by which these neurotoxic species reach the brain have been proposed, and one of these is the bacteria’s use of outer membrane vesicles. This review presents the present evidence of the effects of P. gingivalis and its outer membrane vesicles, gingipains, lipopolysaccharide and phosphoglycerol dihydroceramides, on neurodegeneration in neuronal cultures, mice models and post-mortem studies, and determines how this evidence can be used to develop new treatments for AD.

Hepatocellular carcinoma (HCC) is listed as one of the most common causes of cancer-related death. Oncolytic therapy has become a promising treatment because of novel immunotherapies and gene editing technology, but biosafety concerns remain the biggest limitation for clinical application. We studied the the antitumor activity and biosafety of the wild-type Newcastle disease virus HK84 strain (NDV/HK84) and 10 other NDV strains.

Cell proliferation and apoptosis were determined by cell counting Kit-8 and fluorescein isothiocyanate Annexin V apoptosis assays. Colony formation, wound healing, and a xenograft mouse model were used to evaluate in vivo and in vitro oncolytic effectiveness. The safety of NDV/HK84 was tested in nude mice by an in vivo luciferase imaging system. The replication kinetics of NDV/HK84 in normal tissues and tumors were evaluated by infectious-dose assays in eggs. RNA sequencing analysis was performed to explore NDV/HK84 activity and was validated by quantitative real-time PCR.

The cell counting Kit-8 assays of viability found that the oncolytic activity of the NDV strains differed with the multiplicity of infection (MOI). At an MOI of 20, the oncolytic activity of all NDV strains except the DK/JX/21358/08 strain was >80%. The oncolytic activities of the NDV/HK84 and DK/JX/8224/04 strains were >80% at both MOI=20 and MOI=2. Only NDV/HK84 had >80% oncolytic activities at both MOI=20 and MOI=2. We chose NDV/HK84 as the candidate virus to test the oncolytic effect of NDV in HCC in the in vitro and in vivo experiments. NDV/HK84 killed human SK-HEP-1 HCC cells without affecting healthy cells.

Intratumor infection with NDV/HK84 strains compared with vehicle controls or positive controls indicated that NDV/HK84 strain specifically inhibited HCC without affecting healthy mice. High-throughput RNA sequencing showed that the oncolytic activity of NDV/HK84 was dependent on the activation of type I interferon signaling.

The percentage of vaccinated people in Ukraine and Israel extensively varies. Based on this large difference, the influence of possible collective immunity on the COVID-19 pandemic dynamics in summer 2021 was evaluated.

To clarify the presence of a natural collective immunity, the visible and actual characteristics of the COVID-19 epidemic in Ukraine were estimated based on the number of laboratory-confirmed cases (accumulated in May and June 2021), using a generalized SIR-model and parameter identification procedure, and considering the difference between registered and real number of cases.

The calculated optimal value of the visibility coefficient shows that most Ukrainians have already been infected with coronavirus, some of whom have been infected more than once. This suggests that Ukrainians have probably achieved a natural collective immunity. Despite the large percentage of fully vaccinated people in Israel (approximately 60%), the emergence of a new epidemic wave after June 15, 2021 was not prevented, and the number of deaths increased after July 5, 2021. A new wave of the pandemic in Ukraine after July 10, 2021 is characterized by a smaller daily number of new COVID-19 cases per capita and new deaths per capita, despite having a much lower number of vaccinated people than in Israel. This can be explained by a much lower level of testing (many cases in Ukraine remain undetected) and possibly by the probable natural immunity of Ukrainians.

High levels of vaccination and natural collective immunity are unlikely to prevent new waves of the COVID-19 pandemic caused by mutated coronavirus strains.

The dietary consumption of fructose has increased in the last five decades, paralleled by an increase in obesity. Excess fructose intake is linked to obesity, metabolic syndrome, non-alcoholic fatty liver disease, diabetes, hypertension, cardiac disease, and several aggressive types of cancer. The incidence of acute myeloid leukemia (AML), a lethal hematologic malignancy, has also increased in parallel. Despite significant advances in our understanding of AML, including molecular genetics and more effective targeted therapies, relapse is frequent and outcomes remain poor. Moreover, except for several known causes for a small proportion of AML cases, virtually nothing is known about the initial causative leukemogenic event. In this study, the author asked and intended to answer the question, “can excess fructose intake lead to the initial cellular event that causes AML?” The author reviewed published literature to answer the above question and, subsequently, to identify novel AML therapies based on fructose metabolism. In this article, fructose metabolism and its relationship with metabolic pathways essential for AML, including regulation by hypoxia inducible factor, are described. Evidence for the potential etiologic role of fructose in AML is summarized for the first time. To conclude, excess fructose can lead to the initial AML-causative cellular event. Based on this study, future studies are warranted to determine if restricting fructose intake can prevent AML. Therapeutically, the development of hypoxia inducible factor and glucose transporter 5 inhibitors should be pursued for the treatment of AML.

Intra-abdominal visceral fat accumulation and patatin-like phospholipase domain containing 3 (PNPLA3) rs738409 G/C gene polymorphism confer a greater susceptibility to nonalcoholic fatty liver disease (NAFLD). We examined whether the relationship between visceral fat accumulation and liver disease severity may be influenced by PNPLA3 rs738409 polymorphism.

The variant of PNPLA3 rs738409 was genotyped within 523 Han individuals with biopsy-confirmed NAFLD. Visceral fat area (VFA) was measured by bioelectrical impedance. Significant liver fibrosis (SF), defined as stage F ≥2 on histology, was the outcome measure of interest.

The distribution of PNPLA3 genotypes was CC: 27.5%, CG: 48.2%, and GG: 24.3%. Higher VFA was associated with greater risk of having SF (adjusted-odds ratio [OR]: 1.03; 95% confidence interval [CI]: 1.02–1.04, p<0.05), independent of potential confounders. Among subjects with the same VFA level, the risk of SF was greater among carriers of the rs738409 G genotype than among those who did not. Stratified analysis showed that PNPLA3 rs738409 significantly influenced the association between VFA and SF. VFA remained significantly associated with SF only among the rs738409 G-allele carriers (adjusted-OR: 1.05; 95% CI: 1.03–1.08 for the GG group; and adjusted-OR:1.03; 95% CI: 1.01–1.04 for the GC group). There was a significant interaction between VFA and PNPLA3 rs738409 genotype (Pinteraction=0.004).

PNPLA3 rs738409 G allele has a moderate effect on the association between VFA and risk of SF in adult individuals with biopsy-proven NAFLD. Existence of the PNPLA3 rs738409 G allele and VFA interact to increase risk of SF.

Metabolic (dysfunction)-associated fatty liver disease (MAFLD) affects a third of the population and is a leading cause of liver-related death. Since no effective treatments exist, novel approaches to drug development are required. Unfortunately, outdated terminology and definitions of the disease are hampering efforts to develop new drugs and treatments. An international consensus panel has put forth an influential proposal for the disease to be renamed from nonalcoholic fatty liver disease (NAFLD) to MAFLD, including a proposal for how the disease should be diagnosed. As allies with the many stakeholders in MAFLD care―including patients, patients’ advocates, clinicians, researchers, nurse and allied health groups, regional societies, and others―we are aware of the negative consequences of the NAFLD term and definition. We share the sense of urgency for change and will act in new ways to achieve our goals. Although there is much work to be done to overcome clinical inertia and reverse worrisome recent trends, the MAFLD initiative provides a firm foundation to build on. It provides a roadmap for moving forward toward more efficient care and affordable, sustainable drug and device innovation in MAFLD care. We hope it will bring promising new opportunities for a brighter future for MAFLD care and improve care and outcomes for patients of one of the globe’s largest and costliest public health burdens. From this viewpoint, we have revisited this initiative through the perspectives of drug development and regulatory science.