Necrosis Of Villi Research Articles

Características histopatológicas do intestino delgado e quantificação de bactérias ácido-láticas de frangos de corte suplementados com plectasina

Abstract This study was conducted to determine the histopathological features of the small intestines and to quantify lactic acid bacterial population in the ceca of broiler chickens supplemented with varying doses of plectasin, an antimicrobial peptide with gut health- promoting potentials. This research was done by supplementing broiler chickens with varying doses (150 ppm, 300 ppm and 450 ppm) of plectasin alongside negative and positive control groups. Small intestinal samples showed decreased occurrence and severity of histopathological lesions from the duodenum to the ileum. The occurrence of duodenal lesions such villi necrosis, de-epithelization of villi, haemorrhage and inflammation, observed in the duodenum decreased with supplementation of plectasin, which demonstrated its potential in promoting the structural integrity of the small intestines. On the other hand, microbial enumeration resulted in lower total lactic acid bacteria count in treatment groups supplemented with plectasin, demonstrating its inability to enhance beneficial microbiota, but may be suggestive of improved intestinal absorptive capacity based on the concept of competitive exclusion.

Autophagy increases the survival rate of Macrobrachium rosenbergiiin after Aeromonas hydrophila infection

Autophagy is known as crucial components of crustacean innate immunity against pathogens. The dynamic changes of autophagy level during infectious disease is apparently related to disease severity, which needs to deeply understand for a health development and management of aquaculture. In this study, the role of autophagy during A. hydrophila infection was elucidated in M. rosenbergii. Adult freshwater prawn was firstly administered A. hydrophila to assess the virulence of the isolated strain. Pathological analysis of hepatopancreas and intestine tissues of moribund prawn showed significantly pathological changes, including cellular swelling and vacuolation, contraction or karyorrhexis of nuclei, dissolution and necrosis of villi, structural destruction of the striate border. A significant apoptosis and autophagy was observed in hepatopancreas tissues of the infected shrimp. Moreover, the rapamycin-pretreated groups showed high survival rate in contrast with drastic high mortality in autophagy-suppressed groups. Further analysis showed that the elevated autophagy levels restricted apoptosis signals. We conclude that autophagy plays a positive role during A. hydrophila infection and may be is a new therapeutic target for bacterial disease.

Pathomorphological diagnostics of panleukopenia in cats (case description)

The article highlights the results of autopsy and histopathological studies of cats diagnosed with panleukopenia (FPV), confirmed by immunochromatographic rapid test. The spread of FPV among cats is declining sharply worldwide due to domestic vaccination of cats. However, the number of deaths among homeless animals is still high. The disease course usually varies from subclinical infection to acute syndrome with sudden death. Typical clinical manifestations are characterized by fever, lethargy, and anorexia. Sick cats suffer from vomiting and subsequent watery or hemorrhagic diarrhea. Homeless animals often die from complications associated with secondary bacterial infection, sepsis, and dehydration. Cats aged four months to one year are the most severely affected. Mortality varies depending on the disease course, the animal’s general condition, and timely veterinary care. The autopsy of the dead animals showed signs of catarrhal gastritis, catarrhal and hemorrhagic enterocolitis, splenomegaly, serous lymphadenitis, liver and kidneys’ acute congestive hyperemia, and pulmonary edema. Duodenum histological examination revealed villi necrosis, edema of the mucous membrane’s stroma, and desquamation of enterocytes into the intestinal lumen. Necrosis of Lieberkühn crypts and viral intracytoplasmic inclusions in enterocytes were very pronounced. Microscopic changes in the stomach and large intestine were characterized by dystrophic and necrobiotic changes of mainly the epithelial plate of the mucous membrane. Extracapillary glomerulonephritis developed in the kidneys, while focal emphysema and edema occured in the lungs. Stroma edema, delimphatization and lymphocytic necrosis were observed in the spleen and lymph nodes.

Comparative Comprehensive Analysis on Natural Infections of Hymenolepis Diminuta and Hymenolepis Nana in Commensal Rodents.

SummaryThis first comprehensive report from Punjab province of India relates to patho-physiological alterations alongwith morpho-molecular characterisation and risk assessment of natural infections of Hymenolepis diminuta and Hymenolepis nana in 291commensal rodents including house rat, Rattus rattus (n=201) and lesser bandicoot rat, Bandicota bangalensis (n=90). Small intestine of 53.61 and 64.95 % rats was found infected with H. diminuta and H. nana, respectively with a concurrent infection rate of 50.86 %. There was no association between male and female rats and H. diminuta and H. nana infections (ᵡ2 = 0.016 and 0.08, respectively, d.f.= 1, P>0.05), while the host age had significant effect on prevalence of H. diminuta and H. nana (ᵡ2 = 28.12 and 7.18, respectively, d.f.= 1, P≤0.05) infection. Examination of faecal samples and intestinal contents revealed globular shaped eggs of H. diminuta without polar filaments (76.50 ± 3.01μm x 67.62 ± 2.42 μm), while smaller sized oval eggs of H. nana were with 4 – 8 polar filaments (47.87 ± 1.95 μm x 36.12 ± 3.05 μm). Cestode infection caused enteritis, sloughing of intestinal mucosa, necrosis of villi and inflammatory reaction with infiltration of mononuclear cells in the mucosa and submucosa. Morphometric identification of the adult cestodes recovered from the intestinal lumen was confirmed by molecular characterisation based on nuclear ITS-2 loci which showed a single band of 269 bp and 242 bp for H. diminuta and H. nana, respectively. Pairwise alignment of the ITS-2 regions showed 99.46 % similarity with sequences of H. diminuta from USA and 100 % similarity with sequences of H. nana from Slovakia, Kosice.

Морфологічні особливості системи мати–плацента–плід на фоні інфекцій, що передаються статевим шляхом

The objective: to identify morphological substrate of placental disorders in women with urogenital infections and miscarriages and spontaneous abortions, as well as women diagnosed with «sexually transmitted infections» who gave birth at term. Materials and methods. A morphological study of samples from 80 women of reproductive age was performed. Patients were divided into 4 groups. At the first stage, histological and immunofluorescent studies of abortuses were performed in two groups of women with spontaneous abortions and missed abortions. The I group consisted of samples from 20 patients with urogenital infections, the II group – samples from 20 uninfected women. At the first stage, a morphological (histological and immunofluorescent) study of abortions was performed in two groups of women with missed and spontaneous abortions. The III group consisted of samples from 20 patients with urogenital infections, the IV group (control) – 20 samples from uninfected women. The second stage involved organometric and histostereometric examination of the placenta from women diagnosed with «sexually transmitted infections» without differentiating the forms of the infectious process (main group, n=10), who gave birth at term, and women who were uninfected (control group, n=10) and also gave birth at term. Results. Morphological study of abortuses from infected patients showed that urogenital infections are characterized by pronounced inflammatory changes in the form of deciduitis (9 specimens – 45%); chorionitis (5 specimens – 25%) and syncytial endometritis (2 specimens – 10%). The morphological picture of necrobiosis was revealed in 25% of samples (5 specimens). In addition, amnionitis (6 specimens – 30%), villisitis (4 specimens – 20%) and basal deciduitis (3 specimens – 15%) were detected. In the group of uninfected women, the leading pathomorphological changes were signs of placental immaturity and changes in vascularization and sclerosis of the villi. Most of the studies of placenta and membranes from women who gave birth at term and had urogenital infection showed significant changes in the villous chorion with the involvement of villi of different calibers. There was a significant increase in the proportion of micropathology. The presence of small necrosis of villi was established in almost 1/3 of all cases, extensive areas of necrosis occurred, but there was no significant difference between two groups. There was a decrease in the volume of the chorionic epithelium compared with the control group. Conclusions. Pathomorphological changes of abortuses and placentas in women with STIs reflected the main links in the pathogenesis of infectious and inflammatory processes and were different from such changes in the absence of this pathology. In particular, urogenital infection is characterized by changes associated with inflammatory manifestations in abortuses, and in the group of uninfected women - with signs of placental immaturity and changes in vascularization and sclerosis of the villi. Histostereometry also revealed significant differences in the structure of the placentas of women of the main and control groups, in particular, a significant increase in the proportion of micropathology. Therefore, the prevention of pregnancy complications and pregravid preparation in women diagnosed with STIs is essential for preventing reproductive failures. Keywords: sexually transmitted infections (STIs), spontaneous abortion, missed abortion, placenta, histostereometry.

The protective effect of sodium pyruvate solution to intestinal barrier in hemorrhagic shock rats by intraperitoneal resuscitation

Objective To study the protective effect of sodium pyruvate solution to intestinal barrier in Hemorrhagic shock rats by intraperitoneal resuscitation.Methods A total of 40 Male SD ratswere healthy and clean,were randomly (random number) divided into four groups:sham operation group (group Ⅰ),hemorrhagic shock model group (group Ⅱ),the recovery of the compound sodium chloride intravenous + intraperitoneal recovery of the PD-2 liquid group (group iiⅢ),the recovery of the compound sodium chloride intravenous + sodium pyruvate abdominal recovery group (group Ⅳ) (n =10).In addition to the group Ⅰ,the other three groups are used the HS model by The Wiggers improvement prepared,group Ⅲ,Ⅳ were used the same amount of intravenous recovery,At the same time to the abdominal cavity were respectively injected 20 mL 2.5％ PD-2 liquid and 20 m 2.5％ sodium pymvate solution.After 2 h,each group were taken arterial blood measured arterial blood gases (pH,PaCO2,PaO2) and D-lactic acid,small intestine specimens under the light microscope to observe the morphological changes of the rat small intestinal mucosa.Results Blood gas analysis:group Ⅲ and Ⅳ was significantly increased compared with group Ⅱ in pH levels and PaO2 content (P ＜ 0.01),and comoared to group Ⅲ,pH levels and PO2 levels of group Ⅳ increased more significantly (P ＜ 0.05) ; D-LA content:Group Ⅲ,Ⅳgroup is significantly lower than group Ⅱ (P ＜ 0.01) ; compared with group Ⅲ and group Ⅳ,D-LA significantly decreased (P ＜ 0.05).Light microscope,the group Ⅱ,the rat small intestine layer of a high degree of villous edema,submucosal vascular collapse within the lamina propria glands focal area of necrosis,and large areas of mucosal villi necrosis,defects; group Ⅲ and group Ⅳof small intestinal damage compared to group Ⅱ significantly reduced; Ⅳgroup of the rat small intestine villi edema,lodging and the degree of necrosis in group Ⅲ.Intestinal epithelial damage index score:the Ⅳ group than in group Ⅱ and Ⅲ group (P ＜ 0.01 or P ＜ 0.05).Conclusions The venous recovery and intraperitoneal resuscitation can significantly reduce the plasma D-LA content of hemorrhagic shock in rats,correct acidosis,increase the oxygen partial pressure ; and intestinal mucosal barrier function,the protective of sodium pyruvate solution is better than the PD-2 liquid. Key words: Hemorrhagic shock ; Mucosa abdominal; Intraperitoneal resuscitation; Pyruvate ; D-lactic acid

Hypoxia changes the coagulation capacities of syncytiotrophoblast microparticles (STBM)

Hypoxia changes the coagulation capacities of syncytiotrophoblast microparticles (STBM)

HO-1 expression is not reduced in preeclamptic placenta, and does not regulate sFlt-1 or soluble endoglin secretion in either primary trophoblast or endothelial cells

Results: Histological abnormalities of the three villi populations were observed in the normotensive, mild, moderate and severe hypertensive groups. The occurrence of syncytial knots were observed more frequently in the severely hypertensive than the normotensive group and the moderately hypertensive groups. Fibrinoid necrosis of villi occurred in all villous types in the normotensive group as well as in the hypertensive groups. These areas appeared acidophilic, showing strongly PAS positive necrotic areas of the placental stromal tissue. Complete necrosis of villous stroma was also observed. Hypovascular villi were occasionally observed in all study groups. Thickening of the trophoblast basement membrane was observed in 9 cases of the severely hypertensive group. A semiquantitative increase in the number of villous cytotrophoblast cells were noted in the severely hypertensive group compared to the normotensive group. A nuclear thinned-out area of villous syncytium bulging over the surface of stromal capillaries into the intervillous space was observed in all study groups. Discussion: The histopathological features noted are consistent with hypoxia which emanates from the defective placentation associated with the lack of transformation of the spiral arteries in pre-eclampsia.

Ethanol and age enhances fluoride toxicity through oxidative stress and mitochondrial dysfunctions in rat intestine

Fluoride toxicity and alcohol abuse are the two serious public health problems in many parts of the world. The current study was an attempt to investigate the effect of alcohol administration and age on fluoride toxicity in rat intestine. Six and 18 months old female Sprague Dawley rats were exposed to sodium fluoride (NaF, 25 mg/kg), 30 % ethanol (EtOH, 1 ml/kg), and NaF+EtOH (25 mg/kg+1 ml/kg) for a period of 20, 40, and 90 days. The levels of lipid peroxidation were increased, while the content of reduced glutathione, total, and protein thiol was decreased with NaF treatment. Under these conditions, animals showed an age-related decline in the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione-S-transferase which were further aggravated upon NaF or/and EtOH treatment. Mitochondrial respiration rate and the activities of complexes I, II, and IV enzymes of electron transport chain were decreased, while the levels of nitric oxide and citrulline were increased with age and NaF or/and EtOH treatment. Histological examination revealed large reactive lymphoid follicles, excess of lymphocytes in lamina propria of villi, villous edema, focal ileitis, necrosis of villi, and ulceration in NaF- or/and EtOH-treated animals in both the age groups. These findings suggest that fluoride mediate its toxic effects on intestine through oxidative stress and mitochondrial dysfunctions which are further augmented with alcohol consumption and advancing age.

Placental Histopathological Changes Associated with Plasmodium vivax Infection during Pregnancy

Histological evidence of Plasmodium in the placenta is indicative of placental malaria, a condition associated with severe outcomes for mother and child. Histological lesions found in placentas from Plasmodium-exposed women include syncytial knotting, syncytial rupture, thickening of the placental barrier, necrosis of villous tissue and intervillositis. These histological changes have been associated with P. falciparum infections, but little is known about the contribution of P. vivax to such changes. We conducted a cross-sectional study with pregnant women at delivery and assigned them to three groups according to their Plasmodium exposure during pregnancy: no Plasmodium exposure (n = 41), P. vivax exposure (n = 59) or P. falciparum exposure (n = 19). We evaluated their placentas for signs of Plasmodium and placental lesions using ten histological parameters: syncytial knotting, syncytial rupture, placental barrier thickness, villi necrosis, intervillous space area, intervillous leucocytes, intervillous mononucleates, intervillous polymorphonucleates, parasitized erythrocytes and hemozoin. Placentas from P. vivax-exposed women showed little evidence of Plasmodium or hemozoin but still exhibited more lesions than placentas from women not exposed to Plasmodium, especially when infections occurred twice or more during pregnancy. In the Brazilian state of Acre, where diagnosis and primary treatment are readily available and placental lesions occur in the absence of detected placental parasites, relying on the presence of Plasmodium in the placenta to evaluate Plasmodium-induced placental pathology is not feasible. Multivariate logistic analysis revealed that syncytial knotting (odds ratio [OR], 4.21, P = 0.045), placental barrier thickness (OR, 25.59, P = 0.021) and mononuclear cells (OR, 4.02, P = 0.046) were increased in placentas from P. vivax-exposed women when compared to women not exposed to Plasmodium during pregnancy. A vivax-score was developed using these three parameters (and not evidence of Plasmodium) that differentiates between placentas from P. vivax-exposed and unexposed women. This score illustrates the importance of adequate management of P. vivax malaria during pregnancy.

Modulation of lipid peroxidation and antioxidant defense systems in rat intestine by subchronic fluoride and ethanol administration

Excessive consumption of fluoride and ethanol has been identified as injurious to human health. Fluoride and ethanol co-exposures are commonly seen among the alcoholics residing in endemic fluoride areas worldwide. This study was undertaken to examine the modulation of lipid peroxidation and antioxidant defense systems in rat intestine by subchronic fluoride and ethanol administration. Female Sprague-Dawley rats were divided into four groups: group I (control), group II (fluoride was given orally at a dose of 25 mg/kg body weight), group III (30% ethanol was given orally at a dose of 1 mL/kg body weight), and group IV (a combination of fluoride and ethanol was administered orally at the dose described for groups II and III). Lipid peroxidation was elevated ( P < .05) in intestine of rats by fluoride or ethanol treatments for 20 or 40 days. However, glutathione content was reduced by fluoride (32 and 44%) and ethanol (21 and 40%) treatments after 20 and 40 days, respectively. Fluoride-exposed animals showed reduction ( P < .05) in the activities of superoxide dismutase (22 and 42%), catalase (30 and 37%), glutathione peroxidase (22 and 35%), glutathione reductase (32 and 34%), and glutathione- S-transferase (24 and 30%) after 20 and 40 days. A similar decrease ( P < .05) in the activities of these enzymes was also noticed in animals exposed to ethanol for 20 or 40 days. The observed changes in lipid peroxidation, reduced glutathione levels, and enzyme systems were further augmented in intestine of rats exposed to fluoride and ethanol together. Intestinal histology showed large reactive lymphoid follicles along with mild excess of lymphocytes in lamina propria of villi, villous edema, focal ileitis, and necrosis of villi in animals exposed to fluoride and ethanol for 40 days. These findings suggest that fluoride and ethanol exposure induces considerable changes in lipid peroxidation, antioxidant defense, and morphology of rat intestine, which may affect its functions.

Morphological changesof the gutas the result of acutehemorrhage

In experiment on rats morphological changes of the gut depending on life expectancy as the result of acute hemorrhage have been studied. During the first day in mucous tunic of the small intestine reduction of its thickness, desquamation and necrosis of villi were marked, in 7,4 % of cases there were erosions and ulcers. The quantity of mast cells with degranulation attributes was increasing from 3 o'clock till 7 o'clock, eosinophilic leukocytes - from 12 o'clock till 24 o'clock. As a result dystrophic changes in ganglion cells of vegetative nervous textures and in smooth muscle cells of a muscle coat led to paresis of the intestine. Changes in the small intestine were characterized by greater expressiveness of dystrophic and necrotic injuries in comparison with the large intestine

The therapeutic effect of recombinant human trefoil factor 3 on hypoxia-induced necrotizing enterocolitis in immature rat

Trefoil peptides are a new class of regulatory peptides involved in mucosal protection and repair in the gastrointestinal tract. Among them, trefoil factor 3 (TFF3) (intestinal trefoil factor) is known to be cytoprotective in the gut. The aim of this study was to determine the effect of recombinant human trefoil factor 3 (rhTFF3) on hypoxia-induced necrotizing enterocolitis (NEC) in immature rats. In the present study, thirty-two 1-day-old Wistar rat pups were randomly divided into four groups. Group 1 served as nonhypoxic controls. Group 2 rats were subjected to hypoxia reoxygenation (H/O) and then were returned to their mothers. Groups 3 and 4 rats were subjected to H/O, were returned to their mothers, and were treated with rhTFF3 intraperitoneally (0.5 mg) and subcutaneously (0.2 mg), respectively, for the next 3 days. All animals were killed on day 4, and intestine specimens were obtained to determine the histological changes, tissue level of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), prostaglandin E2 (PGE2), tromboxane B2 (TXB2), and nitric oxide (NO). In addition, the effects of rhTFF3 on abundance of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) were also investigated. In neonatal NEC (group 2), necrosis of villi and crypts and, in some cases, transmural necrosis was observed under light microscopy. Tissue level of interleukin-8, tumor necrosis factor-α, malondialdehyde, prostaglandin E2, tromboxane B2, and nitric oxide were significantly higher than group 1. In addition, abundance of inducible nitric oxide synthase and cyclooxygenase 2 was markedly increased. In groups 3 and 4, only very slight intestinal injury was observed. The tissue level of interleukin-8, tumor necrosis factor-α, malondialdehyde, prostaglandin E2, tromboxane B2, and nitric oxide were significantly decreased in comparison to the group 2. Meanwhile, the abundance of inducible nitric oxide synthase and cyclooxygenase 2 was also marked decreased in comparison to group 2. The current study suggests a therapeutic role of TFF3 in an experimental model of NEC. Our findings may open a new insight into the treatment of NEC in newborns.

Relevance of Irinotecan Hydrochloride-Induced Diarrhea to the Level of Prostaglandin E2 and Water Absorption of Large Intestine in Rats

For characterization of the mechanism(s) of severe diarrhea due to the anticancer agent, irinotecan hydrochloride (CPT-11), examination was made of the relation of CPT-11-related diarrhea to colonic prostaglandin E2 (PGE2) and water absorption in rats. Acute diarrheal symptoms were observed within 1 hr after the administration of CPT-11 to rats, with increased PGE2 and decreased water absorption in the colon. Treatment with atropine at 1 mg/kg, s.c. was noted to inhibit intestinal PGE2 and the CPT-11-related acute diarrheal symptoms, indicating that these diarrheal symptoms were mediated through the cholinergic nervous system accelerated functionally by CPT-11. On the other hand, daily treatment of CPT-11 at the same dose resulted in chronic diarrheal symptoms in all animals 3 days after CPT-11 treatment. Histopathological changes observed in the descending colon and ileum of the rats included degeneration and necrosis of villi and cryptal cells and a decrease in the number of the goblet cells. Significantly increased PGE2 and impaired water absorption of the descending colon were also observed during the chronic diarrheal stage. It can be considered that the chronic diarrheal symptoms appear as a consequence of the gastrointestinal injury characterized by significant increase in PGE2 accompanied by impaired water absorption.

17 OXYGEN RADICALS STIMULATE PROSTAGLANDIN SYNTHESIS IN THE RAT SMALL INTESTINE

We studied the effects of oxygen radicals produced by Hypoxanthine(Hx) and xanthine Oxidase(XO) on the rat small intestine to see whether this model could mimic the intestinal damage seen in infants with Necrotizing Enterocolitis(NEC). In anesthetised rats the ilium was divided with a silk suture preserving the blood supply into eight 5cm long segments. Each loop was injected with 0,5ml of Ringer acetat or Hx 1mM/l dissolved in Ringer plus 0, 1, 2 or 5 units of XO. After 2 hours the animals were sacrificed, the loops of the intestine taken out, and the following parameters measured: Fluid volume(ml), electrocytes(mmol/l) and prostaglandins(pg/0,1ml) in the intestinal fluid. Results: The intestines were also studied by light microscopy: In rats given 5u of XO there was haemorrhage into mucosa and muscularis propria with necrosis of villi. Several of the rats showed pronounced oedema. These findings were considerably less marked with smaller concentrations of XO(p≤0,05). The present model demonstrates that the Hx/XO system potently affects biochemical functions of the small intestine. With high concentrations of XO the mucosa, the muscularis propria and the villi are damaged, and we speculate whether this might represent the pathogenesis of NEC. Further, these experiments suggest that oxygen radicals can stimulate prostaglandin synthesis in the small intestine.

Debris Observed by Arthroscopy of the Knee

In examination of 732 knee joints through the arthroscope since 1961, various types of debris were observed in 47. The debris was classified into four groups: precipitation of fibrin, degeneration and necrosis of villi, desquamation of articular cartilage, and metaplasia of villi. Diseases of the knee joint and their pathogenesis are discussed in the light of these findings.