Infected Liver Research Articles

Microplastics exacerbate tissue damage and promote carcinogenesis following liver infection in mice

Cancer is a leading cause of death worldwide, posing a substantial threat to human well-being. Microplastics (MPs) exposure can harm human health and the carcinogenicity of MP remains uncertain. In this study, we investigated carcinogenesis by MPs exposure. We observed MP significantly exacerbated hepatic injury in infectious conditions. In addition, cancer-related p53 and p21 signals are activated by MPs. Analysis of the liver transcriptomic landscape uncovered a noteworthy intensification of the carcinogenesis pathway by MPs compared with pre-infection. The transcription factor SALL2 could act as an oncogenic promoter in the promotion of cancer regulated by MPs. Further, big data analysis presents the correlation between MPs pollution and human hepatocellular carcinoma. This work revealed a toxic amplification effect of the non-bioactive MPs on the bioactive pathogens. This finding provides new insight into understanding the potential toxicity of the MPs.

Hepatitis B viral infection and its common genotype circulation: A molecular approach

Hepatitis B virus (HBV) is the causes of liver infection and associated with cirrhosis, carcinoma, and fibrosis of liver. In this research study, we conducted an observational study to evaluate the distribution of HBV infection and its genotypes in selected cities of Khyber Pakhtunkhwa, Pakistan. A total of 426 samples were collected from selected cities of Khyber Pakhtunkhwa. Mardan (n = 163), Dir (Lower) (n = 116), Malakand (n = 53), Miran Shah (n = 29), Dera Ismail Khan (n = 28), Swat (n = 22), and Hangu (n = 15). For molecular identification of hepatitis B virus infection, the ICT (Immunochromatographic techniques) kits were used for the Screening of Hepatitis B virus infection among general population. The positive samples of ICT test were further subjected to Real-time Polymerase chain reaction (PCR), of which 282 (66.2 %) were males, and 144 (33.8 %) were females. Out of 426 ICT kit positive samples, 218 (51.18 %) were found PCR positive. The maximum number of positive cases, 157 (36.86 %), was found between 15 and 34 years. Sixty samples were further processed for HBV genotyping. A mixed genotype was detected in 29 (48.3 %) individuals, followed by genotype D in 23 (38.3 %) and untypable in 8 (13.3 %). The positivity rate of HBV was recorded high among males compared to females. Most patients who reported positive for HBV were co-infected with two genotypes. This research will help to provide background information to government and health authorities to raise public awareness and improve the capacity of the healthcare delivery system for hepatitis B virus infection.

Roles of X-box binding protein 1 in liver pathogenesis.

The prevalence of drug-induced liver injury (DILI) and viral liver infections presents significant challenges in modern healthcare and contributes to considerable morbidity and mortality worldwide. Concurrently, metabolic dysfunction-associated fatty liver disease (MAFLD) has emerged as a major public health concern, reflecting the increasing rates of obesity and leading to more severe complications such as fibrosis and hepatocellular carcinoma. X-box binding protein 1 (XBP1) is a distinct transcription factor with a basic-region leucine zipper structure, whose activity is regulated by alternative splicing in response to disruptions in endoplasmic reticulum (ER) homeostasis and the unfolded protein response (UPR) activation. XBP1 interacts with a key signaling component of the highly conserved UPR and is critical in determining cell fate when responding to ER stress in liver diseases. This review aims to elucidate the emerging roles and molecular mechanisms of XBP1 in liver pathogenesis, focusing on its involvement in DILI, viral liver infections, MAFLD, fibrosis/cirrhosis, and liver cancer. Understanding the multifaceted functions of XBP1 in these liver diseases offers insights into potential therapeutic strategies to restore ER homeostasis and mitigate liver damage.

Effect of Temperature and Salinity on Survival of Protoscoleces of Hydatid Cyst in Liver In Vitro.

Hydatid cyst is the metacestode stage of Echinococcus granulosus that occurs in herbivores and humans as intermediate hosts by consuming parasite eggs through forage and vegetables. Carnivores, as definitive hosts, become infected by consuming infected vesicles of herbivores. The most effective treatment for a hydatid cyst is surgical operation. Inactivating E. granulosus protoscoleces through heating, cooling, or chemicals such as sodium chloride can be considered an effective method for controlling hydatidosis in both humans and animals. The main objective of this study was to evaluate the effect of different temperatures and salinity conditions on the survival of Echinococcus granulosus protoscoleces. For this purpose, 50 g of infected liver (in triplicate) was separately treated with different temperatures (+10°C, +50°C, +60°C, +72°C, and -20°C) and concentrations of sodium chloride (5%, 10%, 15%, and 20%) for 3, 6, 12, 24, 48, and 72 h. Additionally, 50 g of infected liver was stored separately in the refrigerator (+4°C) as a control group. The survival rate of the protoscoleces was evaluated by staining with 1% eosin under a light microscope. The results showed that the protoscoleces were significantly affected, with 100% mortality at -20°C after 0.5 h, and complete death at +72°C, +60°C, +50°C, and +10°C after 1, 1.5, 3, and 24 h, respectively (p < 0.005). Similarly, the protoscoleces in the liver mass survived at 5% NaCl after 3 h but died at 10% after 24 h, at 15% after 12 h, and at 20% after 6 h. It is concluded that exposing the liver infected with protoscoleces hydatid cyst to a temperature of -20°C and a sodium chloride concentration of 10% for 24 h is suitable for inactivating the protoscoleces.

Chronic Viral Infections and Hepatic Oncogenesis

Hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis D virus (HDV) are major contrib¬utors to chronic liver disease and hepatocellular carcinoma (HCC) worldwide. Discovered in the 1960s and 1980s, these viruses are associated with significant global health burdens. HBV, a member of the He¬padnaviridae family, is a partially double-stranded DNA virus responsible for chronic liver infections that can lead to HCC. Despite the success of HBV vaccination, challenges such as vaccine escape mutants and non-responders persist. HCV, a member of the Flaviviridae family and a positive-sense single-stranded RNA virus, affects millions globally. While direct-acting antivirals (DAAs) can achieve high rates of viral clearance, vaccine development remains hindered by genetic diversity and immune evasion. HDV, the smallest known human virus, relies on HBV for its propagation. It exacerbates liver disease and increases HCC risk, particularly in co-infected individuals. HDV does not integrate into the host genome, suggesting indirect mechanisms of carcinogenesis, potentially through interactions with HBV. Addressing these chal¬lenges requires enhanced vaccination strategies, improved antiviral therapies, and continued research to understand the complex interplay between these viruses and liver cancer development.

Multi-step synthesis, kinetics and in silico explorations of indole-Phenyl-1,2,4-triazole Bi-heterocyclic hybrids unified with 3-substituted benzamides as elastase inhibitors

In the present research work, a library of unique indole-phenyltriazole hybrids comprising 3-substituted-benzamide moiety was synthesized through convergent multi-step strategy. The structural confirmation of all synthesized molecules was corroborated by IR, 1H NMR, 13C MMR, EI-MS and CHN analysis data. The results of in vitro inhibitory potential of novel benzamides against elastase enzyme revealed that all molecules were potent inhibitors and 10d was most active compound among them having IC50 value of (0.197 ± 0.027 µM), relative to the standard (13.421 ± 0.016 µM). The Kinetics mechanism analyzed by Lineweaver-Burk plots which exposed that 10d inhibited this enzyme competitively by forming an enzyme-inhibitor complex. The inhibition constant Ki determined from Dixon plot for compound 10d was 0.85 µM. Moreover, cytotoxicity of these compounds was also profiled by hemolytic activity and it was observed that almost all these benzamides compounds displayed low cytotoxicity. These molecules also exhibited mild cytotoxicity toward red blood cell membrane. In addition, the in silico computational explorations fully supported the in vitro enzyme inhibitory results. The binding energy ranges from -7.1 to -9.1 kcal/mol, which showed that compound possessed good interaction tendencies to the pancreatic elastase target protein. So, it was anticipated from the experimental results and computational investigations of the current research that these derivatives might lead to further research gateways for obtaining better and safe nontoxic medicinal scaffolds for dealing with the elastase related ailments such as lungs diseases, pruritic skin disease and liver infection.

Hepatitis B Virus X Protein Induces Reactive Oxygen Species Generation via Activation of p53 in Human Hepatoma Cells.

Hepatitis B virus (HBV), particularly through the HBx protein, induces oxidative stress during liver infections. This study reveals that HBx increases reactive oxygen species (ROS) via two distinct mechanisms. The first mechanism is p53-independent, likely involving mitochondrial dysfunction, as demonstrated by elevated ROS levels in p53-deficient Hep3B cells and p53-knocked-down HepG2 cells after HBx expression or HBV infection. The increase in ROS persisted even when p53 transcriptional activity was inhibited by pifithrin-α (PFT-α), a p53 inhibitor. The second mechanism is p53-dependent, wherein HBx activates p53, which then amplifies ROS production through a feedback loop involving ROS and p53. The ability of HBx to elevate ROS levels was higher in HepG2 than in Hep3B cells. Knocking down p53 in HepG2 cells lowered ROS levels, while ectopic p53 expression in Hep3B cells raised ROS. HBx-activated p53 downregulated catalase and upregulated manganese-dependent superoxide dismutase, contributing to ROS amplification. The transcriptional activity of p53 was crucial for these effects, as cells with a p53 R175H mutation or those treated with PFT-α generated less ROS. Additionally, HBx variants with Ser-101 increased p53 and ROS levels, whereas variants with Pro-101 did not. These dual mechanisms of HBx-induced ROS generation are likely significant in the pathogenesis of HBV and may contribute to liver diseases, including hepatocellular carcinoma.

Characterizing Unique Clinical and Virological Profiles in Concurrent Chronic Hepatitis B and Metabolic Dysfunction-Associated Liver Disease: Insights from a Population-Based Cohort Study.

Background: The concurrent presence of chronic hepatitis B virus (CHB) infection and metabolic dysfunction-associated steatotic liver disease (MASLD) presents a unique clinical scenario with implications that are not yet fully understood. This study aims to characterize the distinct clinical and virological features of CHB in the context of MASLD and evaluate its impact on disease progression and outcomes. Methods: Utilizing a comprehensive health maintenance organization database, this study included 1186 patients with CHB from 2000-2020. Patients were categorized into two groups: CHB-MASLD (n = 188) and CHB alone (n = 998). CHB diagnosis was confirmed by serological markers, while MASLD was diagnosed based on imaging and cardiometabolic risk factors. Comparative analysis and multiple regression models were applied to assess variables related to viral parameters and clinical outcomes. Results: The CHB-MASLD group was older (mean age of 45.2 vs. 39.1, p < 0.001) with higher rates of obesity (46.8% vs. 23.8%, p < 0.001), diabetes (36.2% vs. 17.3%, p < 0.001), and dyslipidemia. Distinct viral profiles included higher HBeAg negativity (96.2%), a higher rate of HBeAg-negative infection (70.4% vs. 63.8%; p < 0.001), and increased HBeAg seroconversion under treatment. Cirrhosis was more prevalent in the CHB-MASLD group (9.6% vs. 4.4%, p = 0.007), while HCC rates were comparable. Multivariate analysis identified age, male gender, chronic active hepatitis, and diabetes as predictors of cirrhosis. Conclusions: CHB-MASLD patients were distinguished by a higher prevalence of metabolic features, along with a distinct viral profile marked by increased chronic HBeAg infection, higher rates of HBeAg seroconversion, and a potential association with worse disease outcomes.

Morphological and molecular identification of Euclinostomum heterostomum (Trematoda: Clinostomidae) from spotted snakehead Channa punctata in Bangladesh.

Parasites belonging to the trematode family Clinostomidae have a global distribution. Freshwater fish in Bangladesh frequently serve as hosts for different clinostomid species. During the metacercaria stage, the digenetic trematode Euclinostomum heterostomum exhibits a specific preference for Channidae species, where it undergoes encystment within the liver, kidneys, and muscles of these hosts. The study aimed to identify E. heterostomum in Channa punctata through combined morphological and molecular analysis. Light and scanning electron microscopy were conducted to investigate the morphological characteristics of the species. The histological examination of the infected liver tissue revealed the presence of encysted flukes, inflammatory leukocyte infiltrates, and degeneration and loosening of hepatic tissue. In molecular analysis, the generated internal transcribed spacer 1 (ITS1), 5.8S ribosomal DNA and ITS2 regions sequence (GenBank accession no: OR591452) of 830 bp showed 100% identity with Euclinostomum heterostomum identified in India (MT785786). The phylogenetic reconstruction provided substantial evidence of genetic similarities (0-1% genetic distance) among different isolates of the genus Euclinostomum, suggesting that there is a shared heritage.

No impact of HIV coinfection on the mortality in patients with hepatitis C virus infection after sustained virological response.

In patients with hepatitis C virus (HCV) chronic infection and advanced liver disease, the impact of human immunodeficiency virus (HIV) coinfection on the clinical outcome after sustained virological response (SVR) has not been sufficiently clarified. The aim of this study was to compare the mortality after SVR of patients bearing HCV chronic infection and advanced liver fibrosis, with and without HIV-coinfection after a prolonged follow-up. This was a prospective multicenter cohort study including individuals with HIV/HCV-coinfection and patients with HCV-monoinfection from Spain, fulfilling: 1) Liver stiffness (LS) ≥9.5 kPa before treatment; 2) SVR with a direct-acting antiviral (DAA) based regimen; 3) LS measurement available at SVR. The main outcome was overall survival. Mortality attributable to liver disease and non-hepatic causes was also assessed. 1,118 patients were included, of whom 676 (60.5%) were living with HIV. The median (Q1-Q3) follow-up was 76 months (57-83). After SVR, 46 (10%) HCV-monoinfected and 74 (11%) HIV/HCV-coinfected patients died. The overall mortality rate (95% CI) was 1.9 (1.6-2.2) per 100 person-years, 1.9 (1.4-2.5) per 100 person-years in patients with HCV-monoinfection and 1.8 (1.6-2.3) per 100 person-years in people living with HIV. In the multivariable analysis, HIV-coinfection was not associated with a shorter survival [0.98 HR (95% confidence interval, CI) = (0.61-1.58), p=0.939]. In patients with HCV chronic infection and advanced fibrosis, HIV-coinfection does not reduce the overall survival after SVR.

Prevalence of bovine fasciolosis and direct financial losses in cattle slaughtered in Bamenda and Bafoussam abattoirs, Western Highlands, Cameroon.

Bovine fascioliasis is a parasitic disease that affects cattle. It leads to direct and indirect great economic loss due to animal mortalities, growth retardation and expenditure on anthelmintics, reduction livestock productivity and essentially condemnation of infected liver by inspection service. The study was carried out to determine the seasonal prevalence and estimated financial losses of fascioliasis in cattle in the Western Highlands of Cameroon. A total of 2167 cattle were selected. Later, the cattle, have being the carcasses, were dissected, and the livers were dissected and carefully examined for adult liver flukes. Faeces were collected immediately after the cattle were killed and examined using the formol-ether concentration technique. Condemned livers were weighted to estimate the financial losses using the average price of a kilogram of liver. A total 428 of cattle were found with infected livers or egg in the faeces giving a total prevalence of 19.75%. Among the infected carcass, 18.64% had both the Fasciola eggs in the faeces and flukes in the liver while 1.10% had only flukes in the liver. Results revealed that prevalence of Fasciola spp. was significantly higher during the rainy season (23.48%) than 16% in the dry season (p=0.00). A significantly (p=0.000) higher prevalence was also observed in females (33.9%) than in males (13.1%). Age range showed significant (p=0.000) influence with the animals of 8-10 years old recorded the highest prevalence of 39.3%. Furthermore, 433.1kg of liver was condemned giving a direct financial loss of 1221,550 FCFA (2049.64 USD) and an annual financial loss due to liver condemnation estimated to 1814,775 (3045.01 USD). Findings of this study indicated that bovine fascioliasis is prevalent in cattle in the Western Highlands of Cameroon, and it leads to an important financial loss particularly in the rainy season.

Kupffer Cells and Hepatocytes: A Key Relation in the Context of Canine Leishmaniasis.

Human zoonotic visceral leishmaniasis (ZVL) and canine leishmaniasis (CanL) constitute a major public and veterinary health concern and are both caused by the infection with the protozoan parasite Leishmania infantum. One of the main target organs in CanL is the liver. This complex organ, composed of various highly specialized cell types, has garnered significant attention from the scientific community as a crucial player in innate immune functions. In the context of CanL, liver infection by parasites and the host immune response generated strongly influence the disease outcome. Thus, taking advantage of a co-culture system involving canine hepatocytes and L. infantum-infected autologous Kupffer cells (KCs), allowing cell-to-cell interaction, the current report aims to shed light on the hepatocyte-KCs immune interaction. The co-culture of infected KCs with hepatocytes revealed a vital role of these cells in the activation of a local immune response against L. infantum parasites. Although KCs alone can be immunologically silenced by L. infantum infection, the cell-to-cell interaction with hepatocytes in co-culture can lead to local immune activation. In co-culture it was observed gene expression increased the number of innate immune receptors, specifically cell membrane TLR2 and cytoplasmatic NOD1 along with high TNF-α generation. Altogether, these results suggest that the immune response generated in co-culture could induce the recruitment of other circulating cells to contain and contribute to the resolution of the infection in the liver. This work also enhances our understanding of the liver as a vital organ in innate immunity within the context of CanL.

Chitosan-ricobendazole complex: Synthesis, characterization and anthelmintic activity

Synthesis, characterization and assessment of therapeutic efficacy of chitosan-ricobendazole complex were carried out for the first time in this work. Study of physico-chemical properties revealed the optimal ratio of chitosan: ricobendazole (30:4). Quantum chemical modeling set the optimal parameters for the formation of the chitosan-ricobendazole molecular system (E = −3765.26 kcal/mol, η = 0.127 eV), which was confirmed by Fourier-transform infrared spectroscopy. Scanning electron microscopy showed spherical particles of chitosan-ricobendazole complex ranging in size from 100 to 200 μm. Study of therapeutic efficiency was conducted on sheep with dicroceliosis. Notably, the therapeutic efficiency of the chitosan-ricobendazole complex (4 mg/kg of ricobendazole) reached 89 %, while the therapeutic efficiency of the commercial preparation ricazole (8 mg/kg of ricobendazole) was 92 %. Biochemical blood test indicated equivalent normalization of hematological parameters in sheep after treatment with ricazole and the chitosan-ricobendazole complex. Histological examination of infected sheep liver revealed that treatment with the chitosan-ricobendazole complex leads to a decrease in the number of helminth eggs with subsequent therapeutic effect on the severity of the disease. This proves the enhanced solubility of ricobendazole at a dosage of 4 mg/kg, active interaction of the components and relatively high bioavailability without increasing the release rate of ricobendazole.

Virus-like particle-based vaccines targeting the Anopheles mosquito salivary protein, TRIO.

Malaria is a highly lethal infectious disease caused by Plasmodium parasites. These parasites are transmitted to vertebrate hosts when mosquitoes of the Anopheles genus probe for a blood meal. Sporozoites, the infectious stage of Plasmodium , transit to the liver within hours of injection into the dermis. Vaccine efforts are hindered by the complexity of the parasite's lifecycle and the speed at which the infection is established in the liver. In an effort to enhance immunity against Plasmodium , we produced a virus-like particle (VLP)-based vaccine displaying an epitope of TRIO, an Anopheles salivary protein which has been shown to enhance mobility and dispersal of sporozoites in the dermis. Previous work demonstrated that passive immunization with TRIO offered protection from liver infection and acted synergistically with a Plasmodium targeted vaccine. Immunization of mice with TRIO VLPs resulted in high-titer and long-lasting antibody responses that did not significantly drop for over 18 months post-immunization. TRIO VLPs were similarly immunogenic when combined with an anti-malaria vaccine targeting the L9 epitope of the Plasmodium falciparum circumsporozoite protein.However, when used in a malaria challenge mouse model, TRIO VLPs only provided modest protection from infection and did not boost the protection provided by L9 VLPs.

Sex-specific associations of Notch signaling with chronic HBV infection: a study from Taiwan Biobank

BackgroundHepatitis B, a liver infection caused by the hepatitis B virus (HBV), can develop into a chronic infection that puts patients at high risk of death from cirrhosis and liver cancer. In this study, we aimed to investigate the difference of reactome pre-Notch expression and processing between males and females by using gene to function analysis in FUMA.MethodsWe analyzed Taiwan Biobank (TWB) data pertaining to 48,874 women and 23,178 men individuals which were collected from 2008 to 2019. According to hepatitis B surface antigen (HBsAg) status in hematology, positive and negative were classified into case and control in the genome-wide association study (GWAS) analysis.ResultsWe found 4715 women and 2656 men HBV cases. The genomic risk loci were different between males and females. In male, three risk loci (rs3732421, rs1884575 and Affx-28516147) were detected while eight risk loci (Affx-4564106, rs932745, rs7574865, rs34050244, rs77041685, rs107822, rs2296651 and rs12599402) were found in female. In addition, sex also presented different results. In females, the most significant SNPs are gathered in chromosome 6. However, except for chromosome 6, significant HBV infection SNPs also could be found in chromosome 3 among males. We further investigated gene function in FUMA to identify the difference in reactome pre-Notch expression and processing between males and females. We found that POGLUT1 and HIST1H2BC only appeared in men but not in women.ConclusionAccording to our study, the reactome pre-Notch expression including POGLUT1 and HIST1H2BC was associated with a risk of Hepatitis B in Taiwanese men when compared to women.

Liver-related aspects of valoctocogene roxaparvovec gene therapy for hemophilia A: expert guidance for clinical practice

AbstractAdeno-associated virus–based gene therapy (valoctocogene roxaparvovec) is an attractive treatment for hemophilia A. Careful clinical management is required to minimize the risk of hepatotoxicity, including assessment of baseline liver condition to determine treatment eligibility and monitoring liver function after gene therapy. This article describes recommendations (developed by a group of hemophilia experts) on hepatic function monitoring before and after gene therapy. To prevent harmful liver-related effects, gene therapy is contraindicated in patients with uncontrolled liver infections, autoimmune hepatitis, liver stiffness ≥8 kPa, or cirrhosis. Before using gene therapy in patients with liver steatosis or other liver disorders, the risk of liver damage should be considered using a highly individualized approach. Treatment is not recommended in patients with abnormal liver enzymes, including alanine aminotransferase (ALT) at any level above the upper limit of normal (ULN). Therefore, pretreatment assessment of liver health should include laboratory tests, abdominal ultrasound, and liver stiffness measurements by transient elastography (TE). In the first year after therapy, ALT levels should be monitored 1 to 2 times per week to detect elevations ≥1.5× ULN, which may require immunosuppressant therapy. Patients with ALT elevation should receive prednisone 60 mg/d for 2 weeks, followed by stepwise tapering when ALT returns to baseline. ALT monitoring should continue long term (every 3-6 months), along with abdominal ultrasound (every 6 months) and TE (yearly) evaluations. When patients with good liver health are selected for treatment and closely monitored thereafter, ALT elevations can be promptly treated and are expected to resolve without long-term hepatic sequelae.

Multistage protective anti-CelTOS monoclonal antibodies with cross-species sterile protection against malaria

CelTOS is a malaria vaccine antigen that is conserved in Plasmodium and other apicomplexan parasites and plays a role in cell-traversal. The structural basis and mechanisms of CelTOS-induced protective immunity to parasites are unknown. Here, CelTOS-specific monoclonal antibodies (mAbs) 7g7 and 4h12 demonstrated multistage activity, protecting against liver infection and preventing parasite transmission to mosquitoes. Both mAbs demonstrated cross-species activity with sterile protection against in vivo challenge with transgenic parasites containing either P. falciparum or P. vivax CelTOS, and with transmission reducing activity against P. falciparum. The mAbs prevented CelTOS-mediated pore formation providing insight into the protective mechanisms. X-ray crystallography and mutant-library epitope mapping revealed two distinct broadly conserved neutralizing epitopes. 7g7 bound to a parallel dimer of CelTOS, while 4h12 bound to a novel antiparallel dimer architecture. These findings inform the design of antibody therapies and vaccines and raise the prospect of a single intervention to simultaneously combat P. falciparum and P. vivax malaria.

Clinical Characteristics of Abdominal Infections Caused by Raoultella Spp.: A Retrospective Study.

Background: In recent years, Raoultella spp. have attracted clinical attention as a new type of pathogen. The most common of human infection with Raoultella are bacteremia, urinary tract infections, abdominal infections, etc. Abdominal infection is a serious and complex infection problem. However, there have been no systematic reports of abdominal infections caused by Raoultella. The objective of this study was to explore the clinical characteristics of Raoultella abdominal infections and provide a reference for clinical practice. Methods: A review of publications on abdominal infections caused by the genus Raoultella between 2009 and 2024 is carried out. This review studied seven parameters: infection type, number of cases, gender, age, comorbidities, treatment, and outcome, and descriptive statistical methods were used to analyze the results. Results: A total of 40 cases (16 Raoultella ornithinolytica and 24 Raoultella planticola) were analyzed: 20 cases of biliary tract infection, 5 cases of liver infection, and 4 cases of peritonitis. Fever and abdominal pain were the main symptoms, and some patients present with multiple skin flushes, systemic erythema. Of the 40 cases, 92.5% of patients had underlying diseases. Among them, malignant disease, immunodeficiency, and invasive operations increase the risk of infection. On the basis of the drug susceptibility results, the preferred antibiotics are quinolone, third generations of cephalosporins, carbapenems, and aminoglycoside. Last, patients with abdominal infections caused by Raoultella spp. mostly have a good prognosis after early use of sensitive antibiotics. Conclusions: According to existing literature reports, the main type of abdominal infection caused by Raoultella is biliary tract infection, and most patients have other underlying diseases. Malignancy, immune deficiency, and invasive procedures are risk factors for bacterial infections. This review also emphasizes that Raoultella spp. is a rarely found opportunistic pathogen, which can cause a high incidence of healthcare-associated infections after invasive procedures.

Liver Failure and Cirrhosis Prediction- Using Methods for Machine Learning

Liver disease continues to be a major global health concern, accounting for a considerable portion of global mortality. It results in a variety of symptoms such aberrant nerve function, blood in the cough or vomit, renal and liver failure, jaundice, and liver encephalopathy. It is caused by a myriad of variables that influence the liver, including obesity, untreated hepatitis infection, and alcohol misuse. In order to effectively treat liver infections, early detection is essential, and sensor- based medical technology is frequently used in modern medical procedures to identify illnesses. But diagnosing a condition can be expensive and difficult. Thus, the purpose of this paper is to compare the effectiveness of different machine learning algorithms in order to judge how well they function and have what potential to categorize liver diseases.

Bidirectional relationship between Helicobacter pylori infection and nonalcoholic fatty liver disease: insights from a comprehensive meta-analysis.

Helicobacter pylori (H. pylori) infection and nonalcoholic fatty liver disease (NAFLD) represent significant concerns in global health. However, the precise relationship between H. pylori and NAFLD remains a subject of ongoing debate. This study endeavors to elucidate the association between H. pylori infection and the susceptibility to NAFLD. Furthermore, we aim to investigate the interplay among H. pylori infection, NAFLD, and metabolic syndrome (MetS). We conducted an extensive search of the PubMed, EMBASE, and Web of Science databases spanning from inception to January 2024. Our examination focused on rigorous studies investigating the correlation between H. pylori infection and NAFLD. Utilizing a random-effects model, we computed the pooled odds ratio (OR) and corresponding 95% confidence interval (CI). Additionally, we assessed statistical heterogeneity, performed sensitivity analyses, and scrutinized the potential for publication bias. Thirty-four studies involving 175,575 individuals were included in our meta-analysis. Among these, 14 studies (involving 94,950 patients) demonstrated a higher incidence of NAFLD in H. pylori infection-positive individuals compared to H. pylori infection-negative individuals [RR = 1.17, 95% CI (1.10, 1.24), Z = 4.897, P < 0.001]. Seventeen studies (involving 74,928 patients) indicated a higher positive rate of H. pylori infection in patients with NAFLD compared to those without NAFLD [RR = 1.13, 95% CI (1.02, 1.24), Z = 2.395, P = 0.017]. Sensitivity analyses confirmed the robustness of these findings, and funnel plot analysis revealed no significant publication bias. Furthermore, we observed associations between H. pylori infection or NAFLD and various metabolic factors, including body mass index (BMI), blood pressure, lipids, liver function, and kidney function. Our meta-analysis presents evidence supporting a reciprocal relationship between H. pylori infection and the susceptibility to NAFLD. Nevertheless, additional investigations are warranted to bolster this correlation and unravel the underlying mechanisms involved.