Focal Areas Of Necrosis Research Articles

MICROWAVE ASSISTS HYDROTHERMAL SYNTHESIS OF SOME NANOPARTICLES FOR TARGETED NONINVASIVE OF MALIGNANT CELLS IN GENITAL SYSTEM CAUSING TESTICULAR TUMORS IN MICE

Testicular tumors are the prevailing tumor in male of animals, accounting for about 90% of all tumors affecting the genitalia. Copper nanoparticles (Cu NPs) are emerging as promising agents for cancer therapy. The aim of this work was developed of tumors formed in the testis of mice, by exposure to arsenite (As3) in drinking water for about 6 months and treated by Copper nanoparticles. Twenty male albino Wister mice with average body weight 100 g were used and divided into four groups (five mice / group). Group 1 as control negative group; Gp. 2 (tumor group) injected I/V by Sodium arsenite (0.5 mg/kg) mice once/week for 20 weeks. Gp. 3 (treatment group) gave (Cu NPs.+ Chemotherapy protocol Etopsoide, Cisplatin and Bleomycin every 3 weeks and repeated 3 times; Gp. 4 (chemotherapy group) without Cu NPs. Tissue samples of testis were collected and fixed neutral formalin buffer for histopathology. In the testis of Gp.1 (control group) the seminiferous tubules have the active stages of spermatogenesis with intact germinal epithelium. In Group 2 (tumor Gp.) testicular tumor was formed large yellowish white mass of tumor with hemorrhagic area while in the histopathological examination, testis converted into solid sheet of undifferentiated anaplastic cells showing malignancy with focal areas of necrosis. Gp. 3 (treatment with Cu NPs. + Chemotherapy) was noticed markedly reduce histopathological changes at which the testis appeared neared to normal pattern and active spermatogenesis increased in most of seminiferous tubules as well as restoration of germinal epithelium. Also, interstitial edema was decreased with minimal injury of testicular tissue. Gp.4 chemotherapy treated group, there was no evidence of anaplastic cells; seminiferous tubules showed testicular degeneration with no active spermatogenesis, presence of spermatid giant cells and spermatid coagulum in addition to testicular edema. Finally, nanomaterial will be reduce the toxicity of chemotherapeutics and increase their effectiveness. We need further studies to establish other types of tumors in animals.

Malignant mesothelioma of the tunica vaginalis testis: a rare case and review of literature

BackgroundMalignant mesothelioma of the tunica vaginalis is a rare tumour which comprises less than 1% of all mesotheliomas.Case presentation69-years old patient with painful hard mass and hydrocele in the right scrotum to whom a right hydrocelectomy was performed. Any history of scrotal trauma or exposure to asbestos was not present. Excisional biopsy revealed a multinodular tumour with focal areas of necrosis and infiltrative growth. According to morphological and immunohistochemical findings, diagnosis of malignant biphasic mesothelioma of the tunica vaginalis testis was made. Two months after hydrocelectomy, right inguinal orchidectomy was performed. Post-surgical whole body CT scan revealed paraaortic and pararenal lymphadenopathy, likely to be metastatic. Adjuvant treatment with 6 cycles of cisplatin and pemetrexed was applied. After 3 cycles of chemotherapy, CT scan showed progression and the treatment was changed to gemcitabine 1 month after.ConclusionsAlthough malignant mesothelioma of the tunica vaginalis is a rare malignancy, it poses a diagnostic challenge which can mimic common inguinal or scrotal diseases such as hydrocele. Despite aggressive surgical procedures or adjuvant therapies, the prognosis remains poor.

Mycobacterial antigens accumulation in foamy macrophages in murine pulmonary tuberculosis lesions: Association with necrosis and making of cavities.

Understanding mechanisms of cavitation in tuberculosis (TB) is the missing link that could advance the field towards better control of the infection. Descriptions of human TB suggest that postprimary TB begins as lipid pneumonia of foamy macrophages that undergoes caseating necrosis and fragmentation to produce cavities. This study aimed to investigate the various mycobacterial antigens accumulating in foamy macrophages and their relation to tissue destruction and necrosis. Pulmonary tissues from mice with slowly progressive TB were studied for histopathology, acid-fast bacilli (AFB) and presence of mycobacterial antigens. Digital quantification using Aperio ImageScope was done. Until week 12 postinfection, mice were healthy, and lesions were small with scarce AFB and mycobacterial antigens. Colony-forming units (CFUs) increased exponentially. At week 16-33, mice were sick, macrophages attained foamy appearance with an increase in antigens (P<.05), 1.5 log increase in CFUs and an approximately onefold increase in AFB. At week 37-41, mice started dying with a shift in morphology towards necrosis. A >20-fold increase in mycobacterial antigens was observed with only less than one log increase in CFUs and sevenfold increase in AFB. Secreted antigens were significantly (P<.05) higher compared to cell-wall antigens throughout infection. Focal areas of necrosis were associated with an approximately 40-fold increase in antigen MPT46, functionally active thioredoxin, and a significant increase in all secreted antigens. In conclusion, mycobacterial antigens accumulate in the foamy macrophages in TB lesions during slowly progressive murine pulmonary TB. Secreted antigens and MPT46 correlated with necrosis, thereby implying that they might trigger the formation of cavities.

Pathology and molecular diagnosis of necrotic enteritis in chicken

The present research work was carried out with an aim to study the pathology of necrotic enteritis in chickens followed by isolation and molecular detection of C. perfringens. Total 320 numbers of samples were collected from 15 districts in Assam. Isolation and identification of C. perfringens by cultural, morphological characteristics and confirmation was done by detection of cpa gene of C. perfringens by PCR with virulence toxin genes of C. perfringens such as TpeL and NetB. The clinical signs shown by the birds were diarrhoea, dehydration, depression, reluctance to move, loss of appetite, ruffled feathers, drooping of wings and head and huddling. The gross lesions of intestine revealed haemorrhagic, eroded, detached dead mucosal tissues, diphtheritic membrane, and distention. Liver, kidneys and lungs showed congestion, haemorrhage and focal areas of necrosis. Histopathology of NE in chickens revealed congestion of blood vessels in the lamina propria and submucosa with vacuolation of epithelial cells of intestinal villi with necrosis, making the villi broader and shorter. Different developmental stages of coccidia were also seen in the mucosal epithelial cells in few birds during this study. Liver, kidneys, heart, lungs, spleen, bursa of Fabricius and brain showed variable nature of histopathological lesions like congestion, haemorrhage and focal areas of coagulative necrosis.

Histopathological and histochemical effects of silver nanoparticles on the gills and muscles of African catfish (Clarias garepinus)

This study investigates the effects of silver nanoparticles (AgNPs) and silver nitrate (AgNO3) on gills and muscles in African catfish (Clarias garepinus). Changes in bioaccumulation, histopathological, and histochemical were used as biomarkers. The effects of AgNPs were recorded in some of these properties based on their size (20 and 40 nm) and their concentration (10 and 100 µg/L). The concentrations of silver (Ag) in gills and muscles tissues showed significant variations in all exposed groups compared to the control group. At tissue and cell levels, histopathological changes were observed. These changes include aneurism, collapse, subepithelial edema, epithelium lifting and hyperplasia of interlammellar epithelium, curling of secondary lamellae, epithelial cell necrosis, hypertrophy and proliferation of erythrocytes, bifurcation and fusion of filament, an increase in the number and size of mucous cells in the gills tissues. In addition, degeneration of muscle bundles, infiltration of inflammatory cells, focal areas of necrosis, splitting of muscle fibers, broken myofibrils, thickening of muscle bundles, dislocated striated muscles and shortening of muscle bundles in muscle tissues of fish exposed to AgNPs were exporated to evaluate the changes. Also, depletion of carbohydrates of the gill tissues and the muscle fibers with an increase in the number and size of mucous cells that condense in the secondary lamellae were observed. The 15-day recovery period improved most of the modifications in histopathological and histochemical parameters caused by AgNPs and AgNO3. In conclusion, one can assume the sensitivity of the gills and muscles of C. garepinus to AgNPs and recovery strategy is a must.

1800 Spontaneous Pyomyoma in A Premenopausal Nulliparous Woman without Risk Factors: A Case Report

Study Objective Pyomyoma is a rare complication of leiomyomata that can result in significant morbidity when not diagnosed and treated in timely manner. While most cases occur peripartum, post-uterine instrumentation or following embolization, we report a case of spontaneous pyomyoma with no inciting event necessitating urgent surgical management. Design Case report Setting Academic tertiary care center in Chicago, IL Patients or Participants NA Interventions NA Measurements and Main Results A 49-year-old healthy G0 with known symptomatic myomas presented to the ED with worsening abdominal pain and a blistering, erythematous rash of the right mid abdomen. Her CT demonstrated an enlarged fibroid uterus with an exophytic myoma measuring 28 × 20 × 16cm with focal areas of uterine wall rupture and surrounding fluid and extension into the abdominal wall. Intravenous antibiotics were begun, and she was taken to the operating room. Intraoperatively, she was found to have an enlarged myomatous uterus with a necrotic pedunculated myoma densely adherent to the anterior abdominal wall, gallbladder, liver, omentum, and porta hepatis. The necrotic portion fractured during uterine mobilization and drained more than one liter of purulent fluid. Frozen section was negative for malignancy. An additional suprafascial abscess in the right upper quadrant was drained for an additional 1L of purulent fluid and confirmed infection into the subcutaneous tissue. She underwent a total abdominal hysterectomy, bilateral salpingo-oophorectomy and debulking with residual fibroid capsule seen at the level of the porta hepatis. The patient was discharged home on POD#9; final pathology showed benign degenerated leiomyoma with focal areas of necrosis and inflammation weighing 3538g. Conclusion This is the second case in the literature when a pyomyoma was described in an immunocompetent, premenopausal woman without recent uterine instrumentation. This case highlights how benign myomas may lead to significant morbidity. Although rare, in patients presenting with fever, worsening pain and fibroids, pyomyoma should be considered in the differential.

P.67Overexpression of a constitutively active glycogen synthase in the GSL30 mouse leads to a polyglucosan myopathy

Polyglucosan accumulation is a characteristic feature of several glycogen storage diseases of mammals, including eight in humans and one in horses — the latter associated with a gain of function, through a constitutively active mutant glycogen synthase (GYS1). GSL30 mice overexpressing constitutively active rabbit glycogen synthase in skeletal muscle, accumulate 5-6 times more glycogen in skeletal muscle than wild-type (WT) controls. We hypothesised that this excessive glycogen accumulation would also be associated with a myopathic histological phenotype characterised by polyglucosan accumulation, as seen in GYS1 mutant horses. We examined serum CK activity and skeletal muscle histology from 6 week, 3 month and 8 month old GSL30 mice compared with age-matched WT controls (n=5 to 8). Cryosections from the gastrocnemius, a predominantly fast-twitch muscle, were stained with H&E and amylase-periodic acid Schiff and scored (blinded to genotype) for the presence of internalised nuclei and amylase-resistant polyglucosan within myofibres. Whilst there was no difference in serum CK activity between groups (P>0.05), GSL30 mice had significantly greater numbers of internalised myonuclei than WT controls at 8 months (13.2±6% vs. 0.5%±0.4%; mean±SD; P<0.0001). Polyglucosan was not identified in WT control muscle, but was present increasingly in GSL30 mouse muscle fibres as they aged (reaching 70±5% of myofibres at 8 months). In 6 week old GSL30 mice, amylase-resistant polyglucosan was predominantly subsarcolemmal; by 3 months of age, punctate deposits were identified within the sarcoplasm. By 8 months of age, large pools of glycogen and amylase-resistant polyglucosan, often encompassing the entire myofiber, and focal areas of necrosis were evident. This data reveals that overexpression of glycogen leads to a polyglucosan myopathy in GSL30 mice. Future work will examine the influence of diet and exercise on the phenotype.

Novel SRF-ICA1L Fusions in Cellular Myoid Neoplasms With Potential For Malignant Behavior.

Pericytic tumors comprise a histologic continuum of neoplasms with perivascular myoid differentiation, which includes glomus tumors, myopericytoma, myofibroma, and angioleiomyoma. Despite their morphologic overlap, recent data suggest a dichotomy in their genetic signatures, including recurrent NOTCH gene fusions in glomus tumors and PDGFRB mutations in myofibromas and myopericytomas. Moreover, SRF-RELA fusions have been described in a subset of cellular variants of myofibroma and myopericytoma showing myogenic differentiation. Triggered by an index case of an unclassified cellular myoid tumor showing a novel SRF-ICA1L fusion we have investigated our files for cases showing similar histology and screened them using a combined approach of targeted RNA sequencing and fluorescence in situ hybridization. A fusion between SRF exon 4 and ICA1L exon 10 or 11 was identified in a total of 4 spindle cell tumors with similar clinicopathologic features. Clinically, the tumors were deep-seated and originated in the trunk or proximal lower extremity of adult patients (age range: 23 to 55 y). Histologically, the tumors were composed of cellular fascicles of monomorphic eosinophilic spindle cells showing increased mitotic activity, harboring densely hyalinized stroma, often with focal areas of necrosis. All 4 tumors had similar immunoprofiles with positivity for smooth muscle actin, calponin, and smooth muscle myosin heavy chain. Tumors were negative for desmin and caldesmon, markers often seen in SRF-RELA-positive tumors with similar morphology. Follow-up information was available in 3 patients. Two patients had no evidence of disease, 2 and 5 years after surgical resection. One patient, a 35-year-old male patient with a 19 cm deep-seated tumor with brisk mitotic activity (>20 mitoses in 10 HPF), developed lung metastases 7 years after initial diagnosis. In summary, we report a series of 4 cellular myoid tumors with novel SRF-ICA1L gene fusions, characterized by bland spindle cell fascicular growth, expression of specific smooth muscle markers, elevated mitotic activity, marked stromal hyalinization, focal coagulative necrosis, and potential for malignant behavior. Given the morphologic overlap with related cellular myopericytic tumors with SRF-RELA fusions, it is likely that SRF-ICA1L fusions define a similar subset of neoplasms composed of immature smooth muscle cells.

Human Cytomegalovirus Compromises Development of Cerebral Organoids.

Congenital human cytomegalovirus (HCMV) infection causes a broad spectrum of central and peripheral nervous system disorders, ranging from microcephaly to hearing loss. These ramifications mandate the study of virus-host interactions in neural cells. Neural progenitor cells are permissive for lytic infection. We infected two induced pluripotent stem cell (iPSC) lines and found these more primitive cells to be susceptible to infection but not permissive. Differentiation of infected iPSCs induced de novo expression of viral antigens. iPSCs can be cultured in three dimensions to generate cerebral organoids, closely mimicking in vivo development. Mock- or HCMV-infected iPSCs were subjected to a cerebral organoid generation protocol. HCMV IE1 protein was detected in virus-infected organoids at 52 days postinfection. Absent a significant effect on organoid size, infection induced regions of necrosis and the presence of large vacuoles and cysts. Perhaps more in parallel with the subtler manifestations of HCMV-induced birth defects, infection dramatically altered neurological development of organoids, decreasing the number of developing and fully formed cortical structure sites, with associated changes in the architectural organization and depth of lamination within these structures, and manifesting aberrant expression of the neural marker β-tubulin III. Our observations parallel published descriptions of infected clinical samples, which often contain only sparse antigen-positive foci yet display areas of focal necrosis and cellular loss, delayed maturation, and abnormal cortical lamination. The parallels between pathologies present in clinical specimens and the highly tractable three-dimensional (3D) organoid system demonstrate the utility of this system in modeling host-virus interactions and HCMV-induced birth defects.IMPORTANCE Human cytomegalovirus (HCMV) is a leading cause of central nervous system birth defects, ranging from microcephaly to hearing impairment. Recent literature has provided descriptions of delayed and abnormal maturation of developing cortical tissue in infected clinical specimens. We have found that infected induced pluripotent stem cells can be differentiated into three-dimensional, viral protein-expressing cerebral organoids. Virus-infected organoids displayed dramatic alterations in development compared to those of mock-infected controls. Development in these organoids closely paralleled observations in HCMV-infected clinical samples. Infection induced regions of necrosis, the presence of larger vacuoles and cysts, changes in the architectural organization of cortical structures, aberrant expression of the neural marker β-tubulin III, and an overall reduction in numbers of cortical structure sites. We found clear parallels between the pathologies of clinical specimens and virus-infected organoids, demonstrating the utility of this highly tractable system for future investigations of HCMV-induced birth defects.

MORPHOLOGICAL CHANGES IN THE SMALL INTESTINE OF RATS WITH ACUTE GENERALIZED PERITONITIS

The main cause of mortality in acute generalized peritonitis (AGP) is the development of multiple organ insufficiency. The intestine is the organ where the first changes develop in this pathology.&#x0D; The aim of the study – to research and evaluate the morphological changes in the small intestine wall of animals with experimental AGP.&#x0D; Materials and Methods. 32 white rats were used in this study. Acute peritonitis was modeled by introduction of 10 % fecal suspension in the dosage of 0.5 ml per 100 g of the animal's weight into the abdominal cavity of rats by puncture. The terms of observation: the 1st, 3rd and the 7th days from the beginning of the peritonitis modeling. For histological study the intestinal tissue was taken. The resulting pieces of the organ were fixed in a 10 % neutral formalin solution, which were then stained with hematoxylin and eosin.&#x0D; Results and Discussion. On the 3rd day of the experiment in animals with a modeled AGP, vascular changes were manifested first of all by the rounding (retraction) of endothelial cells or their desquamation and the appearance of defects, that allow plasma proteins and the formed elements of blood to leave circulation boundaries of the vascular bed. On the 7 th day in animals with a modeled AGP increased vascular permeability of the mucous membrane of the small intestine was accompanied by a significant edema of the stroma of the villi and by focal hemorrhages.&#x0D; Conclusion. Consequently, the distinct inflammatory changes in all terms of the injury were seen in the wall of the small intestine at the simulated AGP. The significant expansion of the capillaries and venules against the background of inflammatory infiltration in the stroma of the glandular component of the small intestine was noted on the 1st day from the beginning of the experiment. An increase in the height of intestinal villus and a crypt with retraction and desquamation of endothelial cells in the wall of vessels, which caused platelet adhesion in the areas of destruction was observed on the 3rd day. The areas of focal necrosis of the superficial epithelium, which were accompanied by multiple hemorrhages per diapedesis in the perivascular space of the mucous membrane, were seen in the wall of the small intestine of animals with a simulated AGP on the 7th day.

Immune response and differentially expressed proteins in the lung tissue of BALB/c mice challenged by aerosolized Brucella melitensis 5.

ObjectiveThis study was performed to develop a murine aerosol infection model of brucellosis to investigate the pathogenicity and immune reactions induced by aerosolized Brucella and to identify key proteins associated with Brucella infection in lung tissue.MethodsBALB/c mice were exposed to aerosolized Brucella melitensis 5 (M5) for 30 minutes and killed at 1, 3, 7, and 15 days post-exposure. Clinical observation, pathological analysis of lung tissue, and cytokine expression detection were then performed. Proteomic analysis based on two-dimensional electrophoresis and mass spectrometry was used to identify proteins exhibiting significant changes in expression in lung tissues during Brucella infection.ResultsPathological analysis revealed alveolar wall thickening, telangiectasia with hyperemia, inflammatory cell infiltration, large areas of congestion and bleeding, and areas of focal necrosis. The T-helper 1 type immune response played an important role during aerosol infection, and 12 differentially expressed proteins were involved in the infectious process in lung tissue.ConclusionThese results contribute to our understanding of the pathogenic process of Brucella in the lung tissue of BALB/c mice challenged with aerosolized Brucella. Some of the identified proteins may be potential targets in future therapeutic strategies.

Acute Esophageal Necrosis (AEN)

Introduction: Acute esophageal necrosis (AEN) is a rare finding associated with ischemic changes in the distal third of the esophagus. It is most common in comorbidities that result in hypoperfusion including heart disease, diabetes mellitus, dyslipidemia, hypertension, and renal failure. Case: A 57-year-old female with PMH of DM, COPD, HTN, fibromyalgia, and PAD presented to the ER with a 4 day history of nausea, vomiting, chronic burning chest pain localized to the epigastrium worsening since few days, and abdominal pain. She was not taking her insulin since 4 days. Her home medications include clonidine, Lasix, verapamil, Tressie bowel, Breo, tramadol, Tylenol-codeine, albuterol, and cyclobenzaprine. Surgical history include cholecystectomy and hysterectomy. Physical exam was significant for pain and distress on general exam, rapid deep breathing (Kussmaul), chest wall tenderness, and soft, nondistended, tender epigastrium. Lab values on admission showed mild leukocytosis, pH of 7.22, pCO2 of 12 mmHg, glucose of 447 mg/dL, bicarbonate 37 and potassium of 3.5 mmol/L. CT abdomen and pelvis showed thickening of portions of the stomach and colon suggestive of distention and inflammation, a small hiatal hernia, minimal splenomegaly, and moderate diverticulosis. She was treated with fluid boluses, insulin drip, and potassium replacement for diabetic ketoacidosis (DKA). Over the next 3 days, she had persistent chest pain, intractable vomiting despite multiple antiemetic medications, and small amounts of blood in vomitus. EGD showed severe exudative esophagitis with many areas of focal necrosis suggestive of recent ischemic injury or mucormycosis infection as well as a small hiatal hernia with no evidence of torsion. Biopsy results showed fungal organisms with morphologic features most consistent with Candida and portions of refractile foreign material with no evidence of malignancy. Discussion: Our patient had an atypical presentation as she complained of intermittent odynophagia that worsened during her hospital stay. She was successfully managed with oral PPIs and sucralfate in addition to fluconazole for her candidiasis. Clinicians should be aware of the association between AEN and hypoperfusion or ischemic states including diabetic ketoacidosis as well as bacterial, viral, and fungal infections including esophageal candidiasis.1730_A Figure 1. EGD of severe exudative esophagitis with many areas of focal necrosis1730_B Figure 2. EGD of severe exudative esophagitis with many areas of focal necrosis

Systemic Toxic Reaction Due Bee Stings in Dogs

Background: Toxic reactions due bee stings in human, companion animals, food animals and wild animals are sporadically reported. Accidents involving bees have been occurring in urban and rural areas since 1956, when African bees were introduced in Brazil, forming populations of aggressive hybrid Africanized bees. Their sting cause local and systemicreactions, which include dermatologic reactions, anaphylactic reactions and toxic systemic reactions before death. The aim of this article is to describe the clinical and pathological aspects of the toxic systemic reactions of two dogs that suffered a massive bee attack in the Federal District, Brazil.Cases: A 8-year-old female Brazilian mastiff, and one female 6-year-old Belgian shepherd were locked in the kennel when they suffered a massive bee attack. The dogs presented ‘apathy, congested mucous membranes, dyspnea, epistaxis, hemoglobinuria, icterus (one of them) and convulsions. Clinical pathology results showed a strong hemolyzed plasma, azotemia, leukocytosis with neutrophilia and monocytosis. Both animals were euthanized due to their critical conditions. At necropsy the dogs showed severe subcutaneous edema in the face, moderate congestion of mucous membranes, hematochezia and hematuria. Both dogs presented kidneys dark brown to blackened colored, urinary bladder replete with dark red fluid, lungs severely congested, intestines with severe mural edema and hyperemia containing bloody fecal matter inside, and the liverof one of the dog moderately icteric. The main histologic findings were the moderate diffuse degeneration of the kidney tubular epithelium with small focal areas of necrosis, countless casts of hemoglobin, granular and hyaline casts inside the renal tubules. The skin affected showed stingers inserted, dissociation of the collagen fibers by edema and multifocal areasof hemorrhage, neutrophils and eosinophils, and the muscular tissue underneath had intense necrosis, with hyalinization and moderate multifocal fragmentation of myocytes.Discussion: Africanized bees are well established in rural areas and can adapt to urban areas and, given their marked aggressiveness, cause accidents with animals and humans. Clinical and hematological changes presented by dogs in the DF are similar to those previously reported in this species, which are usually observed in hemolytic anemias and tissuedamage caused by the acute inflammatory response due multiple bee stings. Nephrosis can be considered one of the most important toxic effects, due severe intravascular hemolytic disturbance and rhabdomyolysis, along with acute renal failure caused by the toxin components in the tubules and the toxic-isquemic condition, causing azotemia. Hemolysin proteins such as fosfolipase A and melitina cause rhabdomyolysis, intravascular hemolysis, and hemoglobinemia, which trigger the process of diffuse nephrosis and acute renal failure. The main pathologic changes were observed in the kidneys and skin of the dogs in the DF and were similar to that previously reported in dogs with severe bee stings. The count of inserted bee stingers in the skin and history is considered important to establish a presumptive diagnosis and initiate immediate treatment for the affected animals. The epidemiologic and clinical-pathologic findings presented in these cases are similarto those observed in humans who had suffered systemic toxicity by bee stings and aggravates the general condition of the patient even leading to death. Based on these findings, it was possible to establish the diagnosis of systemic toxic reaction in dogs secondary to poisoning by Africanized bee stings.Keywords: poisonous arthropods, Africanized bees, systemic toxic reaction, toxicology.

Effect of fluoride on major organs with the different time of exposure in rats

BackgroundHigh fluoride levels in drinking water in relation to the prevalence of chronic kidney disease of unknown etiology (CKDu) in Sri Lanka were investigated using rats as an experimental model.MethodThe effects of fluoride after oral administration of Sodium fluoride (NaF) at levels of 0, 0.5, 5 and 20 ppm F− were evaluated in adult male Wistar rats. Thirty-six rats were randomly divided into 4 groups (n = 9), namely, control, test I, II, and III. Control group was given daily 1 ml/rat of distilled water and test groups I, II, and III were treated 1 ml/rat of NaF doses of 0.5, 5, and 20 ppm, respectively, by using a stomach tube. Three rats from the control group and each experimental group were sacrificed after 15, 30, and 60 days following treatment. Serological and histopathological investigations were carried out using blood, kidney, and liver.ResultsNo significant differences were observed in body weight gain and relative organ weights of the liver and kidney in fluoride-treated groups compared to control group. After 60 days of fluoride administration, group I showed a mild portal inflammation with lytic necrosis while multiple areas of focal necrosis and various degrees of portal inflammation were observed in groups II and III. This was further confirmed by increased serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) activities. As compared with control and other treated groups, group III showed a significantly higher serum AST activity (p < 0.05) and ALT activity (p < 0.05) after 60 days and ALP activity with a significant difference (p < 0.05) after 15, 30, and 60 days. The renal histological analysis showed normal histological features in all groups with the elevated serum creatinine levels in group III compared to those in the groups I and II (p < 0.05) after 60 days. Significantly elevated serum fluoride levels were observed in group II of 30 and 60 days and group III after 15, 30, and 60 days with respective to control groups (p < 0.05).ConclusionTaken together, these findings indicate that there can be some alterations in liver enzyme activities at early stages of fluoride intoxication followed by renal damage.

Morphological and functional analyses of skeletal muscles from an immunodeficient animal model of limb-girdle muscular dystrophy type 2E.

ABSTRACT Introduction: Limb‐girdle muscular dystrophy type 2E (LGMD2E) is caused by mutations in the β‐sarcoglycan gene, which is expressed in skeletal, cardiac, and smooth muscles. β‐Sarcoglycan‐deficient (Sgcb‐null) mice develop severe muscular dystrophy and cardiomyopathy with focal areas of necrosis. Methods: In this study we performed morphological (histological and cellular characterization) and functional (isometric tetanic force and fatigue) analyses in dystrophic mice. Comparison studies were carried out in 1‐month‐old (clinical onset of the disease) and 7‐month‐old control mice (C57Bl/6J, Rag2/γc‐null) and immunocompetent and immunodeficient dystrophic mice (Sgcb‐null and Sgcb/Rag2/γc‐null, respectively). Results: We found that the lack of an immunological system resulted in an increase of calcification in striated muscles without impairing extensor digitorum longus muscle performance. Sgcb/Rag2/γc‐null muscles showed a significant reduction of alkaline phosphate‐positive mesoangioblasts. Discussion: The immunological system counteracts skeletal muscle degeneration in the murine model of LGMD2E. Muscle Nerve 58: 133–144, 2018

Cardioprotective effect of camel milk against carbon tetrachloride induced toxicity

Camel milk a nutritional supplement has been known to have anti oxidant properties and has been used for more than a century for treatment of diseases. Twenty adult wistar rats weighing between 150g and 200g were used in the study to determine the protective effective of camel milk on carbon tetrachloride (CCl4) induced cardio‐toxicity in rats. The rats were divided into 5 groups (A, B, C, D and E) of 4 animals each and were fed with rat feed and water for 30days. Control groups (A and B) were injected intraperitoneally (i/p) with 1ml/kgbw of paraffin oil on the 1st and 2nd days, and in addition group B was fed with camel milk for the remaining days. Groups C and D were injected i/p with CCl4 (1ml/kgbw) for 2 consecutive days and group D fed with camel milk for the remaining period. Group E were fed with camel milk and were injected i/p with CCl4 on the last two days.Results showed a decrease in mean body weight of group C significant at p&lt;0.05% while A and B; D and E showed increase in mean body weight. Macroscopically there was loss of normal pericardial outline in group C when compared with the normal. The Histomorphic appearance of cardiac cells in group C showed presence of inflammatory cells, scattered vacuoles and focal areas of necrosis with loss of intercalated disc. The control groups (A and B) and other experimental groups (D and E) appear normal with the preservation of the myocytes.This shows that camel milk is capable of protecting the heart against Carbon tetrachloride Induced toxicity and should be recommended for stress induced disorders.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Evaluation of Fish Health Status and Histopathology in Gills and Liver Due to Metal Contaminated Sediments Exposure

Health status of freshwater fish, Cirrhina mrigala was studied by qualitative and quantitative histopathological analysis, alterations in frequency/prevalence percentages (%) and histological alteration indices (HAI) in response to metal contaminated sediments of the River Ravi aquatic ecosystem. Histo-structures of gill and liver samples of fish were analyzed and comparison between the degree of damage of the alterations in fish organs was performed after exposure to metal contaminated sediments for 7, 14 and 28 days under semi-static water renewal bioassays. Histopathological studies revealed marked histological alterations in the gills and liver of exposed fish as compared to normal tissue structure observed in control fish. The frequency and prevalence percentages observed in 28-day exposed fish were significantly higher as compared to 7- and 14-day exposed fish. The order of frequency and prevalence percentage for gills and liver of exposed fish was as: 28-day > 14-day > 7-day. The highest prevalence percentages recorded were 83 and 80% as focal area of necrosis in gill and liver, respectively, after 28-day exposure. The lowest prevalence percentage observed in 7-day exposed Cirrhina mrigala was dilation of sinusoids (17%).

Effect of Repeated Oral Administration of Roundup® and Ammonium Nitrate on Liver of Wistar Rats

The present study was conducted to evaluate single and interactive toxicity potential of Roundup® and ammonium nitrate in rats for a period of 120 days. Animals of both sexes were divided into four groups of six rats each. Group I served as control and rats were provided with water only. Group II rats were treated orally with Roundup® @ 500 mg/kg b.wt. Rats of Group III were orally administered with ammonium nitrate @ 220 mg/kg b.wt. Group IV received both Roundup® @ 500 mg/kg b.wt and ammonium nitrate @ 220 mg/kg b.wt. Significant increase in plasma alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase was observed in groups II, III and IV as compared to control group I. Liver homogenates manifested significant increase in lipid peroxidation along with significantly decreased activities of superoxide dismutase, catalase and glutathione peroxidase in all treated rats as compared to control. Concomitant exposure to both of these chemicals in group IV showed more significant alterations in various biochemical and oxidative stress indices even in comparison to groups II and III. Histopathologically, Roundup® treated group II showed moderate hepatocytic degeneration and necrosis in liver. Liver in group III showed peri-central mono-nuclear cells (MNC’s) infiltration and focal area of necrosis crowded by mononuclear cells (MNC’s) and in group IV showed severe degeneration of hepatocytes with granular cytoplasm and formation of focal necrotic granuloma infiltrated by mononuclear cells (MNC’s).

Pathological study on urea utilization by poultry

The present work aimed to investigate the histopathological aspects, growth performance, urea residue in muscle and liver of broilerbirds and chemical composition of the breast muscles in birds fed graded levels of urea –treated ration. 80, day old chicks werereared for 6 weeks. After one week of age, chicks were randomly divided into 4 equal groups fed on 1.25%, 2.5%, 5% and 0% ureain their ration. Five birds from each group were sacrificed at the day 7, 14, 28 and 35 from adding urea. The most clinical signswere respiratory symptoms, watery diarrhea and staggering gait. Body weight and feed consumption were increased in group I &II, while the group III showed mild decrease. Urea residue in muscle and liver increased significantly in group III when comparingwith other groups. The chemical composition of the muscle showed that the moisture content in group III was high thangroup IV. There was non-significant increase in the crude protein level in group II. There was significant increase in ashpercent in group II. The fat content in the muscle of all urea treated groups was significant decrease than IV group. Grossly,kidneys and the liver were severe enlarged with pale anemic and mottled coloration. Lungs and the muscles were severe congestedand dark brownish color with petechial and linear hemorrhage in muscle. The brain showed mild hyperemia. Histopathologicalexamination in the kidneys showed degenerative changes in the epithelial cell lining of the renal tubules. The glomeruli showedshrinkages of their glomerular tuft and hyalinization of the Bowman's capsules. Liver showed focal areas of necrosis in the hepaticparenchyma. There was severe thickening of the hepatic capsule. The bile duct showed hyperplasia of their epithelial cell liningwith the presence of desquamated epithelia in the ductile lumen with newly formed bile ductile. Most of hepatic and pulmonaryblood vessels showed thrombosis. Lungs and muscle and brain showed congestion of the blood vessels. The bronchioles showedcatarrhal bronchopneumonia. There was osseous metaplasia among the pulmonary tissue. The neuron was suffering fromTygrloysis with presence of satellotosis and neurophagia. The intestine showed degenerative changes. Myomalecia of some musclecell and suffering from mild degree of hyaline degeneration. It is recommended that lower inclusion levels of urea diets (1.25%)rather than the 2.5% and 5% used in this study be employed for a short period of time.

The ameliorative effect ofAspergillus awamori on aflatoxin B1-induced hepatic damage in rabbits

This study was conducted to investigate the effect of dietary supplementation ofAspergillus awamorion aflatoxin B1(AFB1)-induced liver damage in rabbits. Administration of AFB1(0.3 mg/kg diet) led to a significant reduction in body weight, body weight gain, total feed intake, total serum proteins, albumin, high density lipoprotein-cholesterol, phagocytic activity, phagocytic index, and the antioxidant enzyme, glutathione peroxidase (GPx). Moreover, AFB1administration was associated with a significant increase in feed conversion ratio, lipid peroxidation and serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transferase, lactate dehydrogenase and total bilirubin. In addition, livers of AFB1-supplemented animals showed fatty degeneration with vacuolisation, focal areas of necrosis, mononuclear cells infiltration hyperplasia of bile ducts and sinusoids. A significant increase in the hepatic expression of the biotransformation gene (Cyp3A6), stress-sensitive genes (HO1andSOD1), and inflammation-related genes (IL6, TNFa, NF-kB,andCox2) was also observed. Supplementation of the diets with 0.05, 0.1 or 0.15%A. awamoriameliorated all AFB1deleterious effects with the best improvement observed at the lowest concentration. This is the first investigation to report that supplementation of rabbit diets withA. awamorihas an ameliorative effect against AFB1-induced liver damage possibly through preventing hepatic oxidative stress, promoting the antioxidant defence systems, and inhibiting expression ofCyp3A6,HO1,SOD1,IL6, TNFa, NF-kB,andCox2. Therefore,A. awamoricould be used as a potential preventive or therapeutic agent for aflatoxicosis.