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Pancreatic cancer (PC) is one of the most fatal malignancies, and its incidence and mortality rates are growing annually throughout the world. In this research, we aimed to investigate the time trends and identify the spatial clusters of incidence and mortality on a global scale over the last 30 years, using the Global Burden of Disease (GBD) study 2019 data. Age-standardized incidence and mortality data due to PC were extracted from the GBD study, which was carried out from 1990 to 2019. A Joinpoint regression analysis was utilized to examine trends in the incidence and mortality of PC over the past three decades. As such, spatial analyses were undertaken to detect the spatial distribution and clustering of the metrics globally. It was observed that both the incidence and mortality rates were higher in males than in females worldwide. The global mortality and incidence rates significantly increased by 0.8% per year over the time of follow-up period (p<0.05). By spatial cluster analysis for mortality, European and North African countries, as well as Greenland were explored as hot spots; while South African and Southeast Asian countries were explored as cold spots. Regarding incidence, hot spots were found in European countries, Southern America, and Greenland; whilst cold spots were determined in Southern Africa and Madagascar. Collectively, the temporal trends disclosed a gradual rise in PC incidence and mortality rates over the period 1990-2019, reflecting the global health concern. We further found geographical variations in the patterns and identified high- and low-risk areas for incidence and mortality. These findings facilitate the design and implementation of more resource-efficient and geographically targeted treatments. Given the results of the current study, a practical approach to minimizing the future PC burden involves planned population-wide interventions, as well as primary prevention through healthier lifestyles.

Pancreatic cancer (PC) is an aggressive disease with a high mortality and poor prognosis. The human microbiome is a key factor in many malignancies, having the ability to alter host metabolism and immune responses and participate in tumorigenesis. Gut microbes have an influence on physiological functions of the healthy pancreas and are themselves controlled by pancreatic secretions. An altered oral microbiota may colonize the pancreas and cause local inflammation by the action of its metabolites, which may lead to carcinogenesis. The mechanisms behind dysbiosis and PC development are not completely clear. Herein, we review the complex interactions between PC tumorigenesis and the microbiota, and especially the question, whether and how an altered microbiota induces oncogenomic changes, or vice versa, whether cancer mutations have an impact on microbiota composition. In addition, the role of the microbiota in drug efficacy in PC chemo- and immunotherapies is discussed. Possible future scenarios are the intentional manipulation of the gut microbiota in combination with therapy or the utilization of microbial profiles for the noninvasive screening and monitoring of PC.

Hydatidosis is a disease caused by the larval stage of Echinococcus granulosus, which involves several organs of intermediate hosts. Evidence suggests a communication between hydatid cyst (HC) and hosts via extracellular vesicles. However, a little is known about the communication between EVs derived from HC fluid (HCF) and host cells. In the current study, EVs were isolated using differential centrifugation from sheep HCF and characterized by western blot, electron microscope and size distribution analysis. The uptake of EVs by human monocyte cell line (THP‐1) was evaluated. The effects of EVs on the expression levels of pro‐ and anti‐inflammatory cytokines were investigated using quantitative real‐time PCR (RT‐PCR), 3 and 24 h after incubation. Moreover, the cytokine level of IL‐10 was evaluated in supernatant of THP‐1 cell line at 3 and 24 h. EVs were successfully isolated and showed spherical shape with size distribution at 130.6 nm. After 3 h, the expression levels of pro‐inflammatory cytokine genes (IL1Β, IL15 and IL8) were upregulated, while after 24 h, the expression levels of pro‐inflammatory cytokines were decreased and IL13 gene expression showed upregulation. A statistically significant increase was seen in the levels of IL‐10 after 24 h. The main mechanism of the communication between EVs derived from HCF and their host remains unclear; however, time‐dependent anti‐inflammatory effects in our study suggest that HC may modulate the immune responses via EVs.

The human gastrointestinal (GI) tract harbors gut microbiome, which plays a crucial role in preserving homeostasis at the intestinal host‐microbial interface. Conversely, specific gut microbiota may be altered during various pathological conditions and produce a number of toxic compounds and oncoproteins, in turn, to induce both inflammatory response and carcinogenesis. Recently, promising findings have been documented toward the implementation of certain intestinal microbiome in the next era of cancer biology and cancer immunotherapy. Notably, intestinal microbiota can cooperate with immune checkpoint inhibitors (ICIs) of its host, especially in enhancing the efficacy of programmed death 1 (PD‐1) protein and its ligand programmed death ligand 1 (PD‐L1) blockade therapy for cancer. Herein, we review the dual function of gut microbiota in triggering GI cancers, its association with host immunity and its beneficial functions in modulation of cancer immunotherapy responses. Furthermore, we consider the significance of gut microbiota as a potential biomarker for predicting the efficacy of cancer immunotherapy. Finally, we summarize the relevant limitations that affect the effectiveness and clinical applications of gut microbiome in response to immunotherapy. In this review, we discuss the dual role of gut microbiome in triggering GI cancers, its association with host immunity and its beneficial functions in modulation of cancer immunotherapy responses. Furthermore, we consider the significance of gut microbiota as a potential biomarker for predicting the response to immunotherapy.

This study appraises the psychometrics properties of the Inflammatory bowel disease-fatigue (IBD-F) Persian version questionnaire. The original IBD-F questionnaire was translated into the Persian version in a standard forward-back manner. The validation was performed through the face, content, and construct validity. Fifteen experts scored each item's necessity on an ordinal Likert scale of three; then, the content validity ratio was calculated using the Lawshe formula. Eight judges from pre-defined panel rated each item on an ordinal 4-point Likert scale concerning its relevancy, clarity, and simplicity for individual-CVI calculation. The mean individual-CVI was considered as the Scale-CVI for each domain. Twenty lay experts (selected from the target population) were asked to express their opinion on each item's importance by scoring on a 5-point Likert scale; subsequently, face validity was determined by the impact score formula. The questions that had minimum values of CVR, CVI, and impact score were retained in the final version of the questionnaire for reliability evaluation. Construct validity was evaluated via Confirmatory Factor Analysis. Internal consistency and test-retest reliability were checked using Cronbach's α and intraclass correlation coefficients (ICC). Fifty-four patients recruited based on inclusion and exclusion criteria to participate in the reliability analysis. All the questions received the qualified values of CVR (exceeding 0.49 points) and impact score (more than 1.5 points) and were retained in the questionnaire; however, revisions were made for questions with a CVI 0.7-0.9 for clarity and simplicity. The result demonstrated relative goodness CFA and proper internal consistency, as Cronbach's α coefficient was 0.964 for the test (0.845 and 0.963 for the first and second part of the questionnaire, respectively (and 0.888 for the re-test (0.793 and 0.876 for the first and second section of the questionnaire, respectively). The ICC values between test and re-test for the first and second part and the whole questionnaire were obtained as 0.904, 0.922, and 0.921, respectively. The Persian version of the IBD-F questionnaire was valid and reliable; thus, an appropriate scale was deemed to measure fatigue (severity, frequency, and impact on daily activities).

Gastric cancer is a complex heterogeneous disease with different molecular subtypes that have clinical implications. It is characterized by high mortality rates and limited effective therapies. Microsatellite instability (MSI) has been recognized as a subgroup with a good prognosis based on TCGA and ACRG categorizations. Besides its prognostic and predictive value, gastric cancers with high MSI exhibit different clinical behaviors. The prevalence of high MSI has been assessed in gastric cancer worldwide, especially in East Asia, but there is a lack of such information in the Middle East. Therefore, this study aimed to investigate the incidence and status of MSI in Iranian gastric cancer patients using 53 samples collected from 2015 to 2020 at Taleghani Hospital Medical Center. DNA from tumoral and normal tissues were extracted and assessed through multiplex-PCR based on five mononucleotide repeats panel. Clinicopathological variables, including age, sex, Lauren classification, lymph node involvement, TNM stage, differentiation, localization, and tumor size, were also analyzed. With 2 males and 2 females, high microsatellite instability represented a small subgroup of almost 7.5% of the samples with a median age of 60.5 years. High microsatellite instability phenotypes were significantly associated with patients aged 68 years and older (p‑value of 0.0015) and lower lymph node involvement (p‑value of 0.0004). Microsatellite instability was also more frequent in females, with distal gastric location, bigger tumor size, and in the intestinal type of gastric cancer rather than the diffuse type.

Clostridioides difficile , which causes life-threatening diarrheal disease, is considered an urgent threat to healthcare setting worldwide. The current standards of care solely rely on conventional antibiotic treatment, however, there is a risk of promoting recurrent C. difficile infection (rCDI) because of the emergence of antibiotic-resistant strains. Globally, the alarming spread of antibiotic-resistant strains of C. difficile has resulted in a quest for alternative therapeutics. The use of fecal microbiota transplantation (FMT), which involves direct infusion of fecal suspension from a healthy donor into a diseased recipient, has been approved as a highly efficient therapeutic option for patients with rCDI. Bacteriophages or phages are a group of viruses that can infect and destroy bacterial hosts, and are recognized as the dominant viral component of the human gut microbiome. Accumulating data has demonstrated that phages play a vital role in microbial balance of the human gut microbiome. Recently, phage therapy and fecal virome transplantation (FVT) have been introduced as promising alternatives for the treatment of C. difficile - related infections, in particular drug-resistant CDI. Herein, we review the latest updates on C. difficile - specific phages, and phage-mediated treatments, and highlight the current and future prospects of phage therapy in the management of CDI.

Clostridioides difficile infection (CDI) is one of the most common causes of nosocomial diarrhea in developed countries and the main cause in healthcare settings. This case–control study was designed to evaluate the composition of the gut microbiota dominant bacterial groups in patients with CDI compared to the healthy control subjects. A total of 100 adult subjects involving 50 inpatients with CDI and 50 healthy persons were enrolled in the study. C. difficile isolates were characterized according to the anaerobic culture and presence of toxin genes with multiplex PCR. An ecological analysis was performed real-time quantitative PCR for bacterial elements. The abundances of Enterococcus spp., Lactobacillus spp., Escherichia coli, C. difficile, and Akkermansia muciniphila were higher in group CDI compared with group HC (P < 0.05). The abundances of Bacteroides spp., Bifidobacterium spp., and Faecalibacterium prausnitzii were lower in group CDI than in group HC (P < 0.05). No significant difference was observed in the copy number of Prevotella genus between the CDI and HC subjects (P-value = 0.087). We observed that economic status and income levels were reduced at patients with CDI, however, there was no significant difference between CDI and HC group results and other variables, such as age, BMI, and educational level. These findings showed a reduction in butyrate-producing bacteria and increase in lactic acid-producing bacteria was seen in CDI status. Overrepresentation of Akkermansia may be a predictive marker for the development of nosocomial diarrhea can result in a worse CDI prognosis.

Inflammatory bowel diseases (IBDs) are immune-mediated, chronic relapsing diseases with a rising prevalence worldwide in both adult and pediatric populations. Treatment options for immune-mediated diseases, including IBDs, are traditional steroids, immunomodulators, and biologics, none of which are capable of inducing long-lasting remission in all patients. Dendritic cells (DCs) play a fundamental role in inducing tolerance and regulating T cells and their tolerogenic functions. Hence, modulation of intestinal mucosal immunity by DCs could provide a novel, additional tool for the treatment of IBD. Recent evidence indicates that probiotic bacteria might impact immunomodulation both in vitro and in vivo by regulating DCs’ maturation and producing tolerogenic DCs (tolDCs) which, in turn, might dampen inflammation. In this review, we will discuss this evidence and the mechanisms of action of probiotics and their metabolites in inducing tolDCs in IBDs and some conditions associated with them.