Background Helicobacter pylori infection has been identified to cause constantly recurring inflammation, leading to gastrointestinal tract disorders, including carcinoma. The standard triple therapy (STT), used to eradicate H. pylori, includes two antimicrobials and a proton pump inhibitor for two weeks. Other drug regimens have also been developed since H. pylori exhibits antimicrobial resistance. These regimens, including probiotics, have been shown to lower adverse drug reactions (ADR), improve drug adherence, exert bacteriostatic effect, and reduce inflammation. Objective This study intended to explore probiotic intervention for improving eradication rates and mitigating adverse effects while administrating STT. Methods This prospective study was conducted from May to December, 2021, in the Department of Gastroenterology of Ship International Hospital, Dhaka, Bangladesh, to observe the effects of probiotics inclusion along with STT on H. pylori eradication. A total of 100 patients aged ≥18 years who tested positive for H. pylori were included. The experimental group (n=50) was given STT and probiotics, and the control group (n=50) was given only STT without probiotics for 14 days. Necessary follow-up was done six weeks after treatment. An independent sample t-test, chi-square test, and multiple regression analysis were used for statistical analysis. Result The odds of getting rapid urease test (RUT) negative results from positive were 2.06 times higher (95%CI= 0.95, 3.22, p=0.054) in the experimental group. ADRs were crucially towering in the control group (p=0.045) compared to the probiotics group. The probiotics group had a lower risk of having adverse effects by 0.54 times (95%CI=0.19, 0.84, p=0.032) than the control group. Conclusion Using probiotics and STT together to eradicate H. pylori may lower ADR and improve treatment adherence. It may also help terminate H. pylori infection more effectively. More research is required as H. pylori is very contagious and can ultimately cause life-threatening gastric cancer.
Treatment of resistant obsessive-compulsive disorder (OCD) typically results in insufficient symptom alleviation, and even long-term medication often fails to have the intended effect. Ketamine is a potent non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor. Studies have shown that low-dose ketamine infusion results in a considerable reduction in obsessive-compulsive symptoms and a rapid resolution of suicidal ideation. This is a case report on the effect of intravenous ketamine infusion on a patient with resistant OCD and severe suicidal ideation. Intravenous (IV) ketamine was given once a week over consecutive three weeks with necessary precautions. Psychometric tools such as the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), the Clinical Global Impressions Scale (CGI-S), the Beck Scale for Suicidal Ideations (BSSI), and Depression Anxiety and Stress Scale 21 (DASS-21) were applied before and after infusions. Obsessive-compulsive symptoms and suicidal severity started to decrease rapidly after the first infusion. However, after a transient improvement, these symptoms again began to increase after a stressful incident on the second day of the first infusion. All the symptoms measured by validated rating scales showed continued improvement after the following two infusions. The improvement was sustained until discharge (one week after the last infusion) and subsequent follow-up in the sixth and 12th weeks. The role of ketamine in reducing suicidal thoughts and behavior is already established. Very few studies emphasized its effectiveness in improving severe/resistant obsessive-compulsive symptoms. This pioneering work may offer scope for similar research in the relevant field.
The scientific literature dealing with alcohol and alcoholic beverages revealed that these drinks possess an adverse impact on periodontal tissues. Additionally, other principal risk factors include tobacco, smoking, poor oral hygiene, etc. It has been observed that among chronic alcoholics, there are further issues, such as mental, social, and physical effects, that promote alcoholism. These people may have weak immunity for defense against pathogenic organisms and bacteria. Thus, chances of gingival bleeding, swollen gums, bad breath, and increased bone loss are there. Different alcoholic beverages in the market cause less salivation; these beverages contain sugars that promote acid production in the oral cavity by pathogens that demineralize the enamel and damage gum and teeth. This chronic alcohol consumption can progress into different types of oral disorders, including cancer, halitosis, and caries, and is also associated with tobacco and smoking. Chronic alcohol consumption can cause alteration of the oral microbiome and increase oral pathogens, which lead to periodontal disease and an environment of inflammation created in the body due to malnutrition, diminished immunity, altered liver condition, brain damage, and gut microbiota alteration. Heavily colored alcoholic beverages produce staining on teeth and, due to less saliva, may cause other toxic effects on the periodontium. Over-dependency on alcohol leads to necrotizing lesions such as necrotizing gingivitis, necrotizing periodontitis, and necrotizing stomatitis. These pathological impairments instigate severe damage to oral structures. Therefore, proper counseling by the attending dental surgeon and related health professionals is urgently required for the patient on the basis that the individual case needs to go away from the regular heavy consumption of alcohol.
Human viral oncogenesis is a complex phenomenon and a major contributor to the global cancer burden. Several recent findings revealed cellular and molecular pathways that promote the development and initiation of malignancy when viruses cause an infection. Even, antiviral treatment has become an approach to eliminate the viral infections and prevent the activation of oncogenesis. Therefore, for a better understanding, the molecular pathogenesis of various oncogenic viruses like, hepatitis virus, human immunodeficiency viral (HIV), human papillomavirus (HPV), herpes simplex virus (HSV), and Epstein-Barr virus (EBV), could be explored, especially, to expand many potent antivirals that may escalate the apoptosis of infected malignant cells while sparing normal and healthy ones. Moreover, contemporary therapies, such as engineered antibodies antiviral agents targeting signaling pathways and cell biomarkers, could inhibit viral oncogenesis. This review elaborates the recent advancements in both natural and synthetic antivirals to control viral oncogenesis. The study also highlights the challenges and future perspectives of using antivirals in viral oncogenesis.
The first evidence for the Higgs boson decay to a Z boson and a photon is presented, with a statistical significance of 3.4 standard deviations. The result is derived from a combined analysis of the searches performed by the ATLAS and CMS Collaborations with proton-proton collision datasets collected at the CERN Large Hadron Collider (LHC) from 2015 to 2018. These correspond to integrated luminosities of around 140 fb^{-1} for each experiment, at a center-of-mass energy of 13 TeV. The measured signal yield is 2.2±0.7 times the standard model prediction, and agrees with the theoretical expectation within 1.9 standard deviations.
A combination of fifteen top quark mass measurements performed by the ATLAS and CMS experiments at the LHC is presented. The datasets used correspond to an integrated luminosity of up to 5 and 20 fb^{-1} of proton-proton collisions at center-of-mass energies of 7 and 8 TeV, respectively. The combination includes measurements in top quark pair events that exploit both the semileptonic and hadronic decays of the top quark, and a measurement using events enriched in single top quark production via the electroweak t channel. The combination accounts for the correlations between measurements and achieves an improvement in the total uncertainty of 31% relative to the most precise input measurement. The result is m_{t}=172.52±0.14(stat)±0.30(syst) GeV, with a total uncertainty of 0.33 GeV.
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.