Mild Necrosis Research Articles

Recompensation features and prognosis in hepatitis B virus-related acute-on-chronic liver failure patients.

This study aimed to investigate the characteristics and prognosis of recompensation in hepatitis B virus (HBV)-related acute-on-chronic liver failure (ACLF). A total of 136 patients with HBV-related ACLF were followed up until the end of the study. Patients were categorized into recompensation and non-recompensation groups based on whether recompensation occurred in the first year. The survival rate and incidence of recompensation were calculated using the Kaplan-Meier method. According to the BAVENO VII consensus criteria, 56 (41.18%) of these patients with ACLF regained recompensation in the 1-year follow-up. The recompensated group had less severe liver damage, higher alpha-fetoprotein, lower age, and lower model for end-stage liver disease score. Specifically, in terms of complications, the recompensated group showed a lower incidence compared with the non-recompensated group (P < 0.05). The 3-, 6-, 12-, 36-, and 60-month cumulative survival rates of ACLF were 44.9, 43.4, 43.4, 40.4, and 40.4% respectively. Among the patients who survived beyond 90 days, 57/61 (93.44%) patients showed recompensation of ACLF (with one patient recovering to recompensation after more than 1 year of follow-up), the 3-, 6-, 12-, and 24-month cumulative recompensation rates were 56.5, 90.9, 94.6, and 97.3%, respectively. Among the 57 patients with recompensation of ACLF, 87.7% maintained a stable condition, and 10.5% were diagnosed with hepatocellular carcinoma (HCC). Milder necrosis, less inflammation, and more vigorous hepatic regeneration are conducive to recompensation and a better long-term prognosis in ACLF. However, the occurrence of HCC cannot be avoided and regular monitoring is necessary in the recompensation of ACLF.

Histological and Biochemical Alterations Underlying Statin-Associated Pancreatic Toxicity in a Rat Model

ObjectiveTo investigate the histological and biochemical alterations in the pancreas associated with statin-induced toxicity using a rat model. MethodologyA one-year laboratory-based experimental control trial conducted at department of anatomy of a public sector medical college in Rawalpindi, in collaboration with the National Institute of Health (NIH) Islamabad and Armed Forces Institute of Pathology (AFIP) Rawalpindi. Twenty male Sprague-Dawley rats were assigned to the control group and another twenty to the experimental group. For a duration of 12 weeks, the experimental group was given 60 mg/kg/day of simvastatin orally, whereas the control group was given water and a conventional diet. The following characteristics were measured: body weight, pancreatic weight, biochemical parameters (cytokines, enzymes), and histological alterations (congestion, necrosis, fibrosis). Version 23 of the Statistical Package for the Social Sciences (SPSS) program was used to analyze the data. Qualitative variables were expressed as percentages and frequencies. The statistical significance was defined as P &lt; 0.05. Chi-square analyses contrasted the qualitative factors among the groups. ResultsCompared to controls, the simvastatin group showed significantly increased mean pancreatic weight (p=0.043), congestion (55% vs 0%, p&lt;0.001), higher levels of CRP (p&lt;0.030), IL-6 (p&lt;0.040), and TNF-α (p&lt;0.040). Trends of mild necrosis (25% vs 5%, p=0.182) and interstitial fibrosis (15% vs 0%, p=0.231) were observed but not statistically significant. DiscussionThis work shows that simvastatin significantly affects the pancreatic histomorphology and biochemical parameters in rats. It causes a noticeable amount of necrosis, interstitial fibrosis, and changes the pancreatic biochemical profile. These changes raise the possibility of long-term statin-associated pancreatitis and endocrine/exocrine dysfunction. Using a stable animal model, these new findings offer distinctive insights into the impact of simvastatin on pancreatic morphology. Conclusion Simvastatin profoundly impacts pancreatic histomorphology, warranting further investigation into mechanisms of toxicity and close monitoring of patients for pancreatic adverse effects during statin therapy.

Paracetamol-induced Liver Injury in An Experimental Rat Model: Noninvasive Assessment using DKI and the Effect of Gadoxetate on DKI Parameters.

To explore the potential of diffusion kurtosis imaging (DKI) for assessing the degree of liver injury in a paracetamol-induced rat model and to simultaneously investigate the effect of intravenous gadoxetate on DKI parameters. Paracetamol was used to induce hepatoxicity in 39 rats. The rats were pathologically classified into 3 groups: normal (n=11), mild necrosis (n=18), and moderate necrosis (n=10). DKI was performed before and, 15 min, 25 min, and 45 min after gadoxetate administration. Repeated-measures ANOVA with Tukey's multiple comparison test was used to investigate the effect of gadoxetate on mean diffusivity (MD) and mean diffusion kurtosis (MK) and to assess the differences in MD and MK among the three groups. A receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic accuracy of the MD values when discriminating between the necrotic groups. Gadoxetate had no significant effect on either the MD or the MK, and the effect size was small. The MD in the moderate necrosis group was significantly lower than that in the other two groups (F = 13.502, p < 0.001; η2 = 0.428 [95% CI: 0.082-0.637]), while the MK did not significantly differ among the three groups (F = 2.702, p = 0.081; η2 = 0.131 [95% CI: 0.001-0.4003]). The AUCs of MD for discriminating the moderate necrosis or normal group from the other groups were 0.921 (95% CI: 0.832-1.000) and 0.831 (95% CI: 0.701-0.961), respectively. It would be better to measure the MD and MK before gadoxetate injection. MD showed potential for assessing the degree of liver necrosis in a paracetamol-induced liver injury rat model.

The Potential Value of Mean Platelet Volume and Platelet Distribution Width as Inflammatory Indicators in Surgical Necrotizing Enterocolitis.

This study aims to investigate the potential significance of mean platelet volume (MPV) and platelet distribution width (PDW) in predicting surgical neonatal necrotizing enterocolitis (NEC) and establish the correlation between MPV/PDW levels and the severity/prognosis of NEC. A retrospective study was conducted on a cohort of 372 patients diagnosed with NEC. The patients were categorized into two groups based on whether they underwent surgical therapy. Univariate /multivariate analysis were employed to compare the MPV and PDW between the two groups. Moreover, patients in surgical group were categorized into multiple subgroups based on intraoperative findings and postoperative prognosis, and the levels of MPV and PDW were compared among these subgroups. Of the 372 patients, the operative group exhibited significantly higher levels of MPV and PDW than the nonoperative group (P < 0.05). Logistic regression analysis revealed that MPV (OR = 4.895, P < 0.001) and PDW (OR = 1.476, P < 0.001) independently associated with surgical NEC. The analysis of the receiver operating characteristic (ROC) curve revealed that the area under the curve (AUC) was 0.706 for MPV alone, with a cut-off value of 11.8 fL. Similarly, the AUC was 0.728 for PDW alone, with a cut-off value of 16%. However, when MPV and PDW were combined, the AUC increased to 0.906 for predicting surgical NEC. In accordance with the intraoperative findings, the levels of MPV and PDW were found to be higher in the large area necrosis group than in the partial or mild necrosis group (P < 0.01). Furthermore, the MPV and PDW values in the death group were significantly greater than those in the survival group (P =0.040, P =0.008). MPV and PDW may serve as potentially valuable indicators for determining the need for surgical intervention and predicting the prognosis of patients with NEC.

Synergistic Effect of Naringin and Glimepiride in Streptozotocin-induced Diabetic Rats.

Evaluation of the synergistic effect of Naringin and Glimepiride in streptozotocin (STZ)-induced diabetic rats. Wistar rats were chosen and divided into five groups (n=6). STZ was used for the induction of diabetes. The combination of naringin and glimepiride was administered to diabetic rats. The changes in fasting blood sugar, body weight, Hb, HbA1c, and creatinine were evaluated, and urine was collected and the volume was observed. The lipid profiles like TC, HDL, LDL, and TG were measured. The biochemical parameters SGOT, SGPT, and ALP were analysed. Besides, endogenous antioxidant parameters like SOD, GSH, and catalase were also assessed. Lastly, the histopathological study of the beta cells in islets of the pancreas, glomerulus, and tubules of kidney and liver cells was conducted in all groups. The result shows significant reduction (p<0.001) of blood sugar in the naringin and glimepiride-treated group when compared with the control group (diabetes). Additionally, the combination of Naringin (100 mg/kg) and Glimepiride (0.1 mg/kg) significantly restores the creatinine levels and urine volumes, SGOT, SGPT, and ALP when compared to a single dose of administration. Further, the abnormal lipid profile levels (TC, LDL, TG, and HDL), and endogenous antioxidant enzymes (SOD, GSH, catalase) in diabetic control rats were restored to normal levels in a significant manner. The histopathological result reveals significant alterations, including hypertrophy of islets and mild degeneration, renal necrosis, and inflammation of hepatocytes. A synergistic effect of Naringin and glimepiride was observed during the estimation of various biochemical parameters like body weight, fasting blood sugar, creatinine, urine level, TG, total cholesterol, SGOT, SGPT, ALP, Insulin, HbA1c, antioxidant parameters like SOD, GSH, and catalase in STZ-induced diabetic rats. Further, the combination of therapy improves the protective effect of the pancreas, kidney, and liver, suggesting a potential antidiabetic effect.

Bioactivity, phytochemistry studies and subacute in vivo toxicity of ethanolic leaf extract of white mulberry (Morus alba linn.) in female mice

Ethnopharmacological relevanceTraditional uses of Morus alba L. leaf extracts (MLE) have been reported for treating hyperglycaemia and diabetes. Phytochemical compounds in the leaves demonstrated the ability to enhance insulin sensitivity and β-cell secretory function, suggesting their potential value in reducing blood glucose and treating diabetes. However, the phytochemical constituents and safety of the herbal medicines need to be verified in each experimental field from different growing areas. Studies on the phytochemistry and toxicity of Morus alba leaves in Southeast Asia, especially in Brunei, have never been investigated. Aim of the studyThis study aimed to investigate the bioactivity and phytochemistry of Morus alba ethanolic leaf extract from Brunei Darussalam and its subacute toxic effects in the Institute of Cancer Research (ICR) female mice. Materials and methodsThe phenolic yield and antioxidant of the extract were analysed. Meanwhile, liquid chromatography-mass spectrometry and high-performance liquid chromatography were utilised to determine the phenolic compound of the MLE. In the subacute toxicity study, twenty-five female mice were randomly divided into five groups: the control group, which received oral gavage of 5% dimethyl sulfoxide solvent (DMSO), and the MLE treatment group, which received the extract at a dose of 125, 250, 500 and 1000 mg/kg. Physiology, haematology, biochemistry, and histology were evaluated during the study. ResultsMorus alba leaf depicted total phenolic 10.93 mg gallic acid equivalents (GAE)/g dry weight (DW), flavonoid 256.67 mg quercetin equivalents (QE)/g DW, and antioxidant bioactivity content of 602.03 IC50 μg/mL and 13.21 mg Fe2+/g DW. Twenty compounds in the Morus alba ethanolic leaf extract were identified, with chlorogenic acid (305.60 mg/100 g DW) as the primary compound. As for subacute toxicity in this study, neither mortality nor haematological changes were observed. On the other hand, administration of 500 and 1000 mg/kg MLE resulted in mild hepatocellular injury, as indicated by a significant (p < 0.05) increase in liver enzyme activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). The histopathological score showed mild hepatocellular necrosis in administering 250, 500, and 1000 mg/kg of MLE. The parameters of renal injury were within normal limits, with the increase in eosinophilic cytoplasm observed in the histological scoring at 1000 mg/kg of MLE. ConclusionsMorus alba leaf extract showed abundant polyphenols. In a study on subacute toxicity, MLE caused mild hepatotoxicity in mice. The toxic effect of the extract may be due to kaempferol and chlorogenic acid compounds. The 125 mg/kg MLE dose was safe with no adverse effects.

Hematological, biochemical, and histopathological evaluation of the Morus alba L. leaf extract from Brunei Darussalam: Acute toxicity study in ICR mice.

Studies have reported that the phytochemical content of Mulberry (Morus alba Linn.) is influenced by the area where it grows. On the other hand, the study of the bioactivity and toxicity of mulberry leaves from Brunei Darussalam still needs to be completed. In particular, the investigation regarding the safe dose for Mulberry's application from Brunei Darussalam has yet to be studied. Hence, toxicity information must be considered even though the community has used it for generations. This study investigated Morus alba ethanolic leaf extract (MAE) to observe the acute toxicity in mice. In particular, this study utilized 12 female Institute of Cancer Research mice, 8 weeks old, divided into 2 groups: the control group and the MAE group (2,000 mg/kg single dose). Physiology, hematology, biochemistry, and histology were analyzed during the study. The examination result indicated no mortality and behavioral changes throughout the testing period. However, the mice developed mild anemia and leukopenia, followed by decreased numbers of neutrophils, lymphocytes, and monocytes. In addition, the mice developed a mild hepatocellular injury, indicated by significant (p < 0.05) elevations of both alanine aminotransferase (ALT) and aspartate transaminase (AST). The histopathological findings of the liver were also consistent with the increment of ALT and AST, indicating mild hepatocellular necrosis through the eosinophilic cytoplasm and pyknosis (p > 0.05). It was evident that a single oral administration of MAE was not lethal for mice (LD50, which was higher than 2,000 mg/kg). However, the administration of high doses of MAE must be carefully considered.

Binucleate Rhizoctonia AG‐A causing black root rot of strawberry in Albania

AbstractStrawberry production in Albania is very important and growing rapidly, while data on strawberry diseases are lacking. In 2022, symptoms of leaf necrosis, root rot, and wilt were observed on strawberry plants of cultivars ‘Savana’, ‘Sabrina’, and ‘Fortuna’ in greenhouses near Vajkan, Fier, Albania. The disease incidence was estimated at 50%. Only isolates of Rhizoctonia spp. were obtained from symptomatic plants. The isolates formed fast‐growing, white colonies with binucleate, typically branching hyphae and no sclerotia, resembling Rhizoctonia AG‐A. BLAST analyses of the ITS rDNA of isolate RhizAl (accession number OR231136) revealed the highest nt homology of 99%–100% (100% query coverage) with binucleate Rhizoctonia AG‐A isolates, while the neighbour‐joining phylogenetic analyses confirmed the identification. The pathogenicity of the isolate RhizAl was demonstrated by inoculations of disease‐free strawberry daughter plants (cv. ‘Fortuna’) that developed mild wilting and leaf necrosis 45 days after inoculation while plants collapsed with root necrosis 60 days after inoculation. In this study, binucleate Rhizoctonia AG‐A was detected for the first time as a causal agent of black root rot of strawberries in Albania and in general, and studies on the general importance of Rhizoctonia spp. in different crops in Albania are needed.

Pathological Impacts Due to The Existence of Plastic Waste in Rumen of Bali Cattle

This study aimed to determine the prevalence of Bali cattle rumen containing plastic waste and its impact on tissues and health risks. A total of 100 Bali cattle were investigated after being slaughtered at several traditional slaughterhouses in Denpasar City. Rumen samples were examined for any plastic waste, meanwhile blood, liver, kidney, lungs, spleen, intestine, and myocardium were collected for evaluation of heavy metals content and histopathological examination. The heavy metal measurement was performed using the atomic absorption spectrophotometry (AAS) method. Those tissues for histopathological examination were fixed in buffer neutral formalin (BNF) and then evaluated using hematoxylin-eosin (HE) staining. The results of the examination reported 9 rumens (9%) containing plastic waste. The hematological profile showed leucocytosis and the content of lead (0.841 ± 0.522 ppm). Histopathological changes in the liver, kidneys, lungs, spleen, and intestine, were found in various types of degeneration, inflammation, and mild necrosis. In conclusion, the prevalence of plastic waste in the rumen of Bali cattle was 9%, with leucocytosis, lead content was 0.841 ± 0.522 ppm, and various histopathological lesions such as congestion, inflammation, and fatty degeneration in parenchymous tissues.

Endoplasmic reticulum stress and pro-inflammatory responses induced by phthalate metabolites monoethylhexyl phthalate and monobutyl phthalate in 1.1B4 pancreatic beta cells

In recent years, phthalates and their metabolites have been associated with metabolic diseases such as diabetes mellitus. To investigate the effects of phthalate metabolites exposure on insulin production and release, 1.1B4 pancreatic beta cells were treated with different concentrations (0.001–1000 µM) of monoethylhexyl phthalate (MEHP) and monobutyl phthalate (MBP). For such purpose, the 1.1B4 cells were evaluated for their viability, apoptosis rate, lysosomal membrane permeabilization (LMP), mitochondrial membrane potential (ΔΨm), oxidative stress, ER stress status, in addition to their secretory functions. MEHP, not MBP, exhibited a notable reduction in metabolic viability, particularly at higher concentrations (500 and 1000 µM) following 24-hour exposure. Similarly, both MEHP and MBP induced decreased metabolic viability at high concentrations after 48- and 72-hour exposure. Notably, neither MEHP nor MBP demonstrated a significant impact on apoptosis rates after 24-hour exposure, and MBP induced mild necrosis at 1000 µM concentration. Cell proliferation rates, indicated by PCNA expression, decreased with 10 and 1000 µM MEHP and 0.1 and 10 µM MBP exposures. LMP analysis revealed an increase in 1000 µM MBP group. Exposure to 0.001 µM of both MEHP and MBP significantly reduced cellular glutathione (GSH) levels. No significant change in intracellular reactive oxygen species (ROS) levels and ΔΨm was observed, but MBP-exposed cells exhibited elevated levels of lipid peroxidation. Functional assessments of pancreatic beta cells unveiled reduced insulin secretion at low glucose concentrations following exposure to both MEHP and MBP, with concurrent alterations in the expression levels of key proteins associated with beta cell function, including GLUT1, GCK, PDX1, and MafA. Moreover, MEHP and MBP exposures were associated with alterations in ER stress-related pathways, including JNK, GADD153, and NF-κB expression, as well as PPARα and PPARγ levels. In conclusion, this study provides comprehensive insights into the diverse impacts of MEHP and MBP on 1.1B4 pancreatic beta cells, emphasizing their potential role in modulating cell survival, metabolic function, and stress response pathways.

Prevalence, molecular characterization and the effects of boyprid isopod Probopyrus buitendijki infestation on the Macrobrachium rosenbergii from Nyatoh River, Terengganu, Malaysia

Bopyrid isopod, Probopyrus sp., is an ectoparasite of the freshwater prawn, Macrobrachium spp. The prevalence, morphology, and molecular identity of the parasite collected from Macrobrachium rosenbergii in Nyatoh River, Terengganu, Malaysia were reported herein. Also, the physiological and histological effects of the parasite on the infected prawn were evaluated. A total of 102 M. rosenbergii were collected using both passive and active gears. Out of which thirty-nine samples of the M. rosenbergii, (38.24%) were parasitized by the Probopyrus sp., evident by the visible bulges observed in the prawn’s branchiostegite. Female prawns were observed to have a higher infestation (p < 0.05) than males, while parasitism seemed to be significantly higher (p < 0.05) in middle-sized prawns compared to larger samples. The collected specimen was morphologically suspected to be Probopyrus buitendijki (characterised by a subcordate body that is slightly distorted with five oostegites and black pigment) and was genetically confirmed using 18 S rDNA sequencing. The infested prawn showed a significant reduction (p < 0.05) in hemocyte count and hyaline cells. Significant tissue alterations in the gills and hepatopancreas of the infested prawns were also observed when compared to the control. The various histopathological changes recorded in the infested gills include epithelium lamellae lifting, mild necrosis, hyperplasia of the epithelial cells, pillar cell disruption, and epithelium rupture with haemorrhage. Also, a significant vacuolation of B cells was observed in the infested hepatopancreas compared to the non-infested prawns. It was therefore concluded that the P. buitendijki infestation may strongly correlate with the size and sex of the host and have a significant physiological and histopathological effect on the infested prawns.

Is Intestinal Cell Death in Necrotising Enterocolitis Assorted and Multifarious? A Special Focus on Risk Factors and Their Pathogenic Mechanisms

Necrotising enterocolitis (NEC) is a serious gastrointestinal clinical disorder primarily affecting preterm newborns. It is characterised by a wider histological spectrum, ranging from mild mucosal injury, microvascular thrombosis, and localised necrosis, to transmural intestinal necrosis. In the most severe form, it can be fatal, with complications such as intestinal perforation, peritonitis, and sepsis. Medical management is not clinically efficacious except in mild and self-limiting cases, as it is only focused on symptomatic treatment. Intestinal cell death is regarded as a crucial nascent cellular event in the pathogenesis of NEC that leads to a leaky intestinal barrier, as well as local and systemic inflammation. Therefore, cellular events that besiege intestinal cell death in NEC should be understood in a meticulous and precise manner. This review provides an extensive overview of the different types of cell death in NEC, including apoptosis, necrosis, autophagy, necroptosis, and pyroptosis. This is critically important as it helps us to comprehend the downstream signalling events that play a vital role in the initiation and progression of disease in NEC. Pertinent research studies performed in this regard would unravel novel molecular targets that could form the basis for drafting innovative therapeutic agents for optimising clinical outcomes in NEC.

Is Intestinal Cell Death in Necrotising Enterocolitis Assorted and Multifarious? A Special Focus on Risk Factors and Their Pathogenic Mechanisms

Necrotising enterocolitis (NEC) is a serious gastrointestinal clinical disorder primarily affecting preterm newborns. It is characterised by a wider histological spectrum, ranging from mild mucosal injury, microvascular thrombosis, and localised necrosis, to transmural intestinal necrosis. In the most severe form, it can be fatal, with complications such as intestinal perforation, peritonitis, and sepsis. Medical management is not clinically efficacious except in mild and self-limiting cases, as it is only focused on symptomatic treatment. Intestinal cell death is regarded as a crucial nascent cellular event in the pathogenesis of NEC that leads to a leaky intestinal barrier, as well as local and systemic inflammation. Therefore, cellular events that besiege intestinal cell death in NEC should be understood in a meticulous and precise manner. This review provides an extensive overview of the different types of cell death in NEC, including apoptosis, necrosis, autophagy, necroptosis, and pyroptosis. This is critically important as it helps us to comprehend the downstream signalling events that play a vital role in the initiation and progression of disease in NEC. Pertinent research studies performed in this regard would unravel novel molecular targets that could form the basis for drafting innovative therapeutic agents for optimising clinical outcomes in NEC.

Study of the histopathological and hematological changes due to dimtethoate toxicity in rabbis

The dimethoate is considered as one of most important organophosphorus pesticides that vastly used in agriculture in many countries especially in Iraq which caused different diseases in plants, animals and man. In present study we investigated the histopathological and hematological changes in rabbits resulting from chronic dimethoate intoxication. The treated groups (G2, G3 and G4) received dimethoate orally (10, 25 and 50 mg/kg of B.W.) respectively for two months while the control group (G1) was given water for the same period. The hematological results showed significant decrease in red blood cells counts and hemoglobin values (P&lt; 0.05) in treated groups especially G3 and G4 compared to G1 control group. While the total W.B.Cs counts showed variables values without significant differences between treated groups and control group. The histopathological lesions in organs are dose concerning and include mild hepatocellular degeneration and hepatic necrosis ,hemorrhage with extensive periportal fibrosis, chronic inflammatory cells infiltrations mainly lymphocytes and macrophages in addition to liver fibrosis and cirrhosis and biliary hyperplasia with cholangitis occurred only with toxic doses of dimethoate especially G4, also there degenerative changes and necrosis in kidney and heart, hemosiderosis and hemorrhage with lymphoid depletion in spleen , In brain, there is extensive demyelination and perineruonal edema and perivascular leukocytes cuffing and extensive focal gliosis and the lungs showed congestion with thickened alveolar walls because of slight infiltrations of inflammatory cells mainly lymphocytes and macrophages also there is severe pulmonary hemorrhage and edema with severe emphysematous area and atelectasis in pulmonary tissue. It was concluded that dimethoate induces different histopathological lesions in different organs in rabbits especially in liver which causes hepatocellular degeneration, biliary hyperplasia and cholangitis with hepatic fibrosis and cirrhosis and causes significant decrease in red blood cells counts and hemoglobin values in treated groups compared to the control.

Low alanine aminotransferase activity gene variant in a Siberian Husky with copper-associated hepatopathy

BackgroundAlanine aminotransferase (ALT) is commonly used as a marker of hepatocellular injury. Increased serum ALT activity due to hepatocyte injury occurs in copper-associated hepatopathy (CuCH) and other necroinflammatory liver conditions. Blood ALT concentrations are frequently used to monitor therapy in cases of CuCH. Low serum ALT activities have been associated with an allele at a CFA13 locus.Case presentationA 9-year-old female spayed Siberian Husky was diagnosed with CuCH (hepatic copper dry weight 2680 µg/g [normal, 120–400 µg/g; toxic, > 1500 µg/g]) and a normal ALT (78 U/L; reference range, 10–125 U/L). Mild hepatocellular necrosis was evident histologically. Genetic testing (Embark) revealed that the dog was heterozygous for the low ALT activity gene allele.ConclusionsThis case report illustrates the clinical implications for diagnosing and managing necroinflammatory liver disease such as CuCH in dogs with a low ALT activity genotype.

Relationship between serum biochemical parameters and kidney lesions in broiler chickens with acute tubular necrosis

To evaluate the effectiveness of biochemical factors such as blood urea nitrogen (BUN), creatinine, and serum uric acid in identifying and diagnosing acute tubular necrosis lesion in broilers, kidney tissue and blood samples from 80 broiler chickens at the slaughter stage were collected. Tissue samples were collected in 10% formalin to detect pathological lesions. The components of BUN, creatinine, and serum uric acid were measured with commercially available kits. After preparing the histopathological sections, based on the percentage of necrosis of the kidney tubules in each tissue sample, the pathological lesions were divided into 3 degrees: mild, moderate, and severe. The results showed that 36 samples out of 80 samples (45%) had acute tubular necrosis (ATN) lesions; 14 (17.5%), 12 (15%), and 10 (12.5%) samples had severe, moderate, and mild tubular necrosis lesions, respectively. The amount of uric acid in chickens with moderate and severe lesions showed a significant difference with the chickens without lesions and the mild lesion. However, BUN and creatinine increased significantly only in severe ATN lesions. In general, the results of this study state that severe lesions of renal tubules are associated with an increase in serum BUN, creatinine, and uric acid, but in moderate lesions, only uric acid may increase. Therefore, according to the results of this study, uric acid can be considered as a diagnostic biomarker in moderate to severe ATN.

Histopathological profiles of Albino rats induced with Viscum album leaf and stem aqueous extracts

Background: Viscum album is a hemiparasitic shrub that grows on various tree species and contains diverse active substances. Objectives: The histopathology of the toxic effects of Viscum album leaf and stem aqueous extracts from host plants Azadirachta indica (neem), Psidium guajava (guava), and Acacia albida on organs of albino rats was evaluated. Methodology: Thirty-five (35) albino rats divided into 7 groups (A-G) of 5 albino rats each was exposed to graded doses of 100, 200, 400, 800, 1600, 3200, and 6400mg/kg using the intraperitoneal route. The experimental rats were observed for 24 hours and subsequently sacrificed and their organs including liver, kidney, lungs, and heart were subjected to histopathology for any ultra-structural changes. Results: The histopathological findings indicate that the liver had vacuolar degeneration of hepatocytes and congestion of sinusoids for 800mg/kg of Viscum album (Azadirachta indica: neem) stem extract, and widespread vacuolar degeneration of hepatocytes at 3200mg/kg for Viscum album (Acacia albida) stem extract. The kidneys had congestion, tubular necrosis with deposition of hyaline materials in the intratubular lumen and capsular space of the glomerulus, and glomerular atrophy at 400mg/kg of Viscum album (Psidium guajava: guava) leaf extract, but indicated marked congestion, and tubular necrosis with 3200mg/kg of Viscum album (Psidium guajava: guava) stem. The lungs had marked thickening of the interstitium by edema fluid, red blood, and mononuclear cell infiltration at 3200mg/kg of Viscum album (Acacia albida) leaf extract. The heart had multifocal areas of mild necrosis of the myocytes with 3200mg/kg Viscum album (Azadirachta indica: neem) leaf extract, and multifocal areas of moderate haemorrhages with 3200mg/kg Viscum album (Psidium guajava: guava) leaf extract. Conclusion: Aqueous extracts of Viscum album in this study had bioactive components that could be toxic.

P34 TAKOTSUBO SYNDROME OR UNKNOWN MYOCARDIAL ISCHEMIA? THE ROLE OF CARDIAC MAGNETIC RESONANCE IN DIFFERENTIAL DIAGNOSIS

Abstract There are numerous clinical conditions in which symptoms and signs may overlap, among these myocardial Ischemia in the absence of obstructive coronaropathy (INOCA/MINOCA), gets into differential diagnosis with a plethora of clinical pictures such as Takotsubo syndrome, myocarditis and cardiomyopathies. In this setting, cardiac magnetic resonance has a critical discriminating role. Herein we report the clinical case of a 52–year old patient suffering from hypertension and dyslipidaemia, with a history of chest pain episodes and recent intense psychophysical stress. After symptoms exacerbation, ambulance was called, loss of conscience was witnessed, observing ventricular fibrillation, subjected to prompt DC shock. Once in Emergency room, ECG showed ST–elevation in V1, V2 and AVR for which urgent coronary angiography was performed. It surprisingly resulted negative for epicardial coronary artery disease. Moderate left ventricular dysfunction (LVEF 45%) was found on 2D ultrasound along with apex akinesia, while mild elevation myocardial necrosis enzymes was seen at blood tests. The clinical picture characterized by female sex, history of psychophysical stress, by association of chest pain, ischemic type alterations of repolarization at ECG, akinesia of the apex and the concomitant slight elevation of myocardial necrosis enzymes in the absence of epicardial coronary lesions, highly suggested Tako–Tsubo Syndrome. In order to confirm the diagnosis, cardiac MRI was performed which, unexpectedly, showed the presence of oedema on T2–weighted STIR sequences at the level of the left ventricular apex, associated to same site transmural fibrosis at post–contrast imaging sequences, thus eliciting the hypothesis of a MINOCA. After a new retrosternal pain with transient ST–elevation in V1, a IVUS – guided new coronary angiography examination was performed, resulting intoIVA diffuse coronary spasm, reduced after intravenous nitrate administration. Final diagnosis was “MINOCA complicated by primary VF‘‘ and a subcutaneous AICD implant CMR imaging by virtue of its ability to provide information about cardiac structure and function and simultaneously, to define the characterization of tissues, together with the data of dynamic coronary spasm, proved to be essential in this case to establish the diagnosis, often misunderstood, of MINOCA, hence allowing to define the best therapeutic strategy. ​

Marine toxin C17-SAMT causes major structural damage to vital organs in mice following subchronic toxicity trials

C17-sphinganine analog mycotoxin (C17-SAMT) has been characterized as the contaminant responsible for the atypical toxicity reported in mussels from the Bizerte lagoon (northern Tunisia) over the past decade. C17-SAMT exhibited common symptoms of toxicity in mice, including flaccid paralysis and severe respiratory distress, followed by rapid death. To determine the potential health risks of this neurotoxin, we assessed its subchronic toxicity according to the recommendations of OCDE n° 407. The body weight and the structural changes of vital organs were recorded. Biochemical and hematological parameters were also quantified. Macroscopic observations showed that mice treated with 0.9, 9, and 90 µg/kg C17-SAMT had significantly reduced stomach weights, swollen and fragile intestines, and signs of nephritis with renal abscesses. Transaminase assays pointed out that exposure to C17-SAMT can lead to transaminitis. Above-average lactate dehydrogenase values were recorded in both the treated and satellite groups. Hematology data showed a significant reduction in red blood cell counts in high-dose-treated group. Reductions in hemoglobin and hematocrit were also recorded. Mean leukocyte counts were significantly elevated in the high-, mid-dose treated and satellite groups. At the microscopic level, we noted myocardial atrophy and hyperemia. In the lungs, we noted necrosis associated with macrophages perivascular infiltration and congestion. The kidneys showed mild inflammation and glomerular atrophy. The stomach exhibited mucosal atrophy, while a thin colon and distended small intestine were observed in high-dose-treated group. The liver was affected by vascular congestion, inflammatory infiltration, and lobular necrosis that evolved into acute hepatitis. Lesions, such as inflammatory infiltration and mild necrosis of the liver, cortical abscess with central necrosis in the kidney, and mild congestion of cardiac tissue were recorded in the satellite group.

First Report of Neocosmospora Stem Rot of Soybean Caused by Fusarium neocosmosporiellum in Mississippi.

In September 2021, diseased soybean [Glycine max (L.) Merr.] plants were observed in a commercial field in Lamar County, Mississippi (MS). Foliar symptoms included mild interveinal chlorosis and necrosis in the affected plants (Fig. 1a). Stems and roots exhibited orange to black lesions and pith discoloration (Fig. 1b). Signs of the fungus included orange-to-red spherical perithecia, observed in clusters on crowns and roots. Perithecia were surface-sterilized with 70% ethanol for 1 min. Subsequently they were gently pressed in a droplet of 5 μl of sterilized reverse osmosis (RO) water and the suspension was streaked onto potato dextrose agar (PDA) amended with chloramphenicol (75 mg/liter) and streptomycin sulfate (125 mg/liter). Plates were incubated in the dark at 25°C. White to light pink and floccose mycelia developed after four days of incubation and hyaline, one celled, cylindrical to oblong-ellipsoidal microconidia were observed (Fig. 2b; ×400). Conidia measured 8.8 to 19 × 2.8 to 5 μm (n=15). Abundant orange to brown perithecia developed on PDA after three weeks of incubation (Fig. 2a). The asci within the perithecia were cylindrical, eight-spored, thin walled and measured 94.6 to 123.6 μm × 10 to 14 μm (n=10). Ascospores were uniseriate, globose to ellipsoidal, hyaline to brown and measured 11.6 to 16 μm × 7 to 10 μm (n=10; Fig. 2c). The morphological characteristics were consistent with those of Fusarium neocosmosporiellum O'Donnell & Geiser (≅ Neocosmospora vasinfecta E. F. Sm.; Geiser et al. 2013). Genomic DNA was extracted from isolate TW068-21 from a 3-week-old culture plate. The internal transcribed spacer region (ITS), elongation factor 1-alpha (EF1-alpha) and calmodulin (cmdA) gene were amplified, and consensus sequences deposited in GenBank (OM640625, OM681343, OM681344). ITS and EF1-alpha sequence comparison using NCBI BLAST, showed > 99.2% similarity with N. vasinfecta JL2210 while cmdA sequence was 99.8% similar to strain CBS 517.71. A pathogenicity test was performed on 2-week-old Asgrow 46X6 soybean seedlings grown in 10.2 cm pots in a growth chamber. Isolate TW068-21 was grown on antibiotic-amended PDA for 4-weeks and inoculum suspension was prepared with sterilized RO water and adjusted to 2 × 105 ascospores/ml. Soybean seedlings (n=8) were removed from pots and roots were dipped into the inoculum suspension for 20 min. Four control plants were dipped in autoclaved RO water. Plants were re-planted in potting mix, and the inoculated plants were immediately drenched with 20 ml of the inoculum and placed in a growth chamber (25°C; 14 h light). The experiment was repeated once. Inoculated plants presented dark brown discoloration at the base of the stem after 3 weeks of incubation, but no foliar lesions were observed. Control plants remained asymptomatic. Symptomatic stems were placed in a moist chamber (≈23°C; 12 h:h light:dark) and light brown perithecia developed after 1 week. Fusarium neocosmosporiellum was re-isolated from perithecia and stems and colony and spore morphology were similar as described above. To our knowledge, this is the first report of F. neocosmosporiellum in MS. Signs and symptoms of this disease resemble red crown rot. Consequently, careful morphological and molecular assessments should be used for confirmation. Neocosmospora stem rot has been previously reported in Alabama (Gray et al. 1980), Arkansas (Greer et al. 2015), and Georgia (Phillips 1972). Yield losses due to this pathogen in MS are currently unknown.