Placenta percreta in primigravida with unscarred uterus complicated by uterine rupture and sudden maternal and fetal death: an autopsy case report.

Placenta percreta is a rare, aggressive, and severe form of the placenta accreta spectrum. One of its most devastating effects is the sudden rupture of uterus. Uterine scarring is the leading risk factor for uterine rupture, although it can also happen, but rarely, in an unscarred uterus showing more severe repercussions. The present study reported a case of an Egyptian primigravida female, aged 29 years old, at 32 weeks of gestation who died suddenly due to uterine rupture complicating placenta percreta, the diagnosis of which was first settled during autopsy. There was no history of abdominal trauma. No medical history of significance was present. Autopsy denoted an intrauterine fetal death of 32 weeks gestational age. The fundus of the uterus had a laceration (rupture) of the uterine wall including the serosa and myometrium. The placenta has extensively infiltrated the fundus uterine wall and penetrated the myometrium and serosa. Histopathological examination of the ruptured site on the uterus confirms total invasion of the uterine wall by chorionic villi with the presence of hemorrhage and fibrin indicating placenta percreta. Uterine rupture due to placenta percreta may go unnoticed, especially when no associated high-risk factors exist. The current case depicts that placenta percreta is a rare but critical complication of pregnancy that may exist at any stage of pregnancy without any associated high-risk factors with unusual symptoms and leads to uterine rupture and sudden death.

Musa sp. Leaves Extract Ameliorates the Hepato-Renal Toxicities Induced by Cadmium in Mice.

Heavy metals intoxication causes several health problems that necessitate finding new protective and therapeutic approaches. This study aimed to evaluate the impact of Musa sp. leaves extract (MLE) on hepato-renal toxicities induced by cadmium (Cd) in male mice. The phytochemical screening, metal chelating activity (MCA), and the median lethal dose (LD50) of MLE were determined. Fifty CD-1 male mice were used and intraperitoneally (i.p.) injected with MLE (1000 to 5000 mg/kg b.wt) for MLE LD50 determination. Another 50 mice were used for evaluating the effect of MLE on Cd toxicity. Blood samples were collected for hematological, liver, and kidney functions assessments. Liver tissue homogenates were used for determination of oxidant/antioxidant parameters. Liver and kidney tissues were harvested for histopathological and molecular investigations. MLE showed potent in vitro antioxidant activities. The MCA and LD50 of the MLE were 75 µg/mL and 3000 mg/kg b.wt, respectively. MLE showed beneficial therapeutic activity against hepato-renal toxicities in Cd-intoxicated mice, evidenced by improving the hematological, biochemical, histopathological, and molecular alterations.

Ischemic Heart Disease Related Sudden Cardiac Death in Autopsied Cases: An Egyptian perspective.

ABSTRACT: Diagnosis of the underlying cause of sudden unexpected death in a previously healthy individual remains one of the important challenges in forensic practice. Ischemic heart disease is the most common cause of sudden death. The current study aims to investigate the incidence and pathology of sudden ischemic cardiac death in Egypt. All cases of sudden cardiac death (SCD) examined by different forensic departments throughout Egypt during the period of January 2010 through December 2014 were included. Cases underwent complete autopsy examination including a thorough gross and microscopic examination of the heart and great blood vessels. Of 535 cases of SCD diagnosed during the period of the study, coronary atherosclerosis was the principle finding in 420 (78.5%) cases. The highest numbers of deaths were reported in fifth and sixth decades with male preference. Other causes of SCD included myocarditis, cardiomyopathies, valvular heart disease, and hypertensive heart disease (7.8%, 4.1%, 4.1%, and 2.8%, respectively). There was severe stenosis (>75%) of at least 1 coronary artery in 74% of cases. Type VI atherosclerosis was found in 40.7% of cases. The left anterior descending branch was the most affected artery by atherosclerosis. Acute coronary pathological events were demonstrated in 27.6% of cases. Recent myocardial infarction was evident in 55.5% of cases, whereas old infarcts were demonstrated in 44.5% of cases. Features of hypertensive heart disease were present in 18.3% of cases. In conclusion, ischemic heart disease is the leading cause of SCD in Egypt.

Vitamin E supplementation ameliorates the hepatotoxicity induced by Tramadol: toxicological, histological and immunohistochemical study.

Several deleterious effects of Tramadol including deaths were reported especially when used in large doses. Being metabolized mainly in the liver, Tramadol have serious hepatotoxic effects. This study investigates the effect of vitamin E on Tramadol-induced hepatotoxicity in rats by evaluating the antioxidant biochemical markers, the histopathological and immunohistochemical changes.Thirty adult mature male albino rats were divided into five groups (Gs); G1: negative control; G2: received Tramadol 150 mg/kg, G 3-5: received Tramadol plus vitamin E in concentrations of 50 mg/kg, 100 mg/kg and 200 mg/kg respectively. Liver function parameters and oxidative markers in liver tissue (CAT, SOD, GSH, and MDA) were estimated. Liver samples were processed for histopathological and immunohistochemical (Caspase 3 and TNF[Formula: see text]) examinations. The results indicated that Sub-chronic administration of Tramadol resulted in impaired liver functions, increased oxidative stress parameters with decreased antioxidant capacity of liver tissues, severe hepatocellular damage (hydropic degeneration, steatosis and apoptosis) and strong immunoexpression to TNF[Formula: see text] and Caspase 3. All these effects were ameliorated with concomitant administration of vitamin E especially with high doses. The co-treatment of Tramadol-intoxicated rats with Vitamin E, especially in high doses, protects against hepatic toxicity.

Selenium alleviates modafinil-induced neurobehavioral toxicity in rat via PI3K/Akt/mTOR/GSK3B signaling pathway and suppression of oxidative stress and apoptosis: in vivo and in silico study.

Nonmedical use of modafinil (MOD) led to increased rates of overdose toxicity, road accidents, addiction, withdrawal, suicide, and mental illnesses. The current study aims to determine the probable MOD brain toxicity and elucidate the possible role of selenium (Se) in ameliorating the neurotoxicity in rat models. Fifty-four male Albino rats were randomly assigned into nine groups. The groups were G1 (control negative), G2 (Se0.1), G3 (Se0.2), G4 (MOD300), G5 (MOD600), G6 (Se0.1 + MOD300), G7 (Se0.2 + MOD300), G8 (Se0.1 + MOD600), and G9 (Se0.2 + MOD600). After finishing the experiment, blood and brain tissue were harvested for biochemical and histological investigation. Neurobehavior parameters were assessed. Tissue neurotransmitter levels and oxidative stress markers were assessed. Gene expression of PI3K/Akt/mTOR-GSK3B, orexin, and orexin receptor2 was measured by qRT-PCR. Histological and immunohistochemistry assessments, as well as molecular docking, were carried out. MOD-induced neurobehavioral toxicity exhibited by behavioral and cognitive function impairments, which are associated with decreased antioxidant activities, increased MDA levels, and decreases in neurotransmitter levels. Brain levels of mRNA expression of PI3K, Akt, and mTOR were decreased, while GS3K, orexin, and orexin receptors were significantly elevated. These disturbances were confirmed by histopathological brain changes with increased silver and Bax immunostaining and decreased crystal violet levels. MOD induced neurotoxic effects in a dose-dependent manner. Compared with the MOD groups, SE coadministration significantly attenuates MOD-induced toxic changes. Docking study shows the protective role of Se as an apoptosis inhibitor and inflammation inhibitor. In conclusion, Se could be used as a biologically effective antioxidant compound to protect from MOD neurobehavioral toxicity in Wistar rats by reversing behavioral alterations, inflammation, apoptosis, and oxidative injury.

Endomyocardial fibrosis related sudden cardiac death; two autopsied case-reports from Egypt.

Endomyocardial fibrosis (EMF) is an idiopathic tropical disorder that is characterized by the development of restrictive cardiomyopathy. Neglected EMF can cause sudden cardiac death (SCD) in adults. Conclusive diagnosis of EMF depends on autopsy after death. In an effort to attract the interest of the community for this rare disease, we report two cases of SCD that were diagnosed as EMF during autopsy in Egypt. Both cases were thoroughly investigated with emphasis on death circumstances and post-mortem anatomical and histopathological findings. The two cases were for adult males presented with SCD following a quarrel with a negative medical history and family history regarding cardiac diseases. No trauma or drug abuse. The autopsy revealed hypertrophied hearts, thick fibrosed endocardium, patchy myocardial fibrosis, and filling of the apex by fibrosis and calcifications. In one of them, there was a huge mural thrombus reaching the level of the mitral valve that totally occluded the cavity of the left ventricle. Histopathologically, fibrosis was confirmed, and no eosinophils were detected. In contrast to previously reported cases in Egypt, the left ventricle was solely affected. Despite the rarity of the disease outside the tropics, the frequency of EMF cases is more likely to be more than the number of reported cases. EMF should be considered as possible cause of SCD during autopsy. Further studies are needed to clarify the etiology and epidemiology of EMF.

Patterns of acute pediatric intoxication in Aljouf Province, KSA.

Objectives: Although childhood intoxication is avoidable, it remains a leading cause of morbidity and mortality in both developing and developed countries. The aim of this study was to assess the patterns and outcomes of acute pediatric intoxication in Aljouf, KSA. Methods: A retrospective record-based descriptive study was conducted at the Prince Mutaib bin Abdulaziz hospital, and the Maternity and Children's hospital in Aljouf, KSA. All cases of acute intoxication in children younger than 18 years of age from January 1, 2015 to December 31, 2021 were included. Data analysis included demographic characteristics; year and month of intoxication; place, time, form, and route of toxic agent exposure; manner of intoxication; toxic agent/agents involved; intoxicated child's status upon arrival at the hospital; clinical presentation; treatment; admission history; and outcome. Results: A total of 540 cases were reported. Most (79%) acutely intoxicated children were in 1 to <6 years of age. The highest frequency of reported acute pediatric intoxication was 23.9% in 2017. Pharmaceutical drugs were responsible for most reported cases (41%). Most children were asymptomatic (84%) at the time of admission. Among symptomatic children, GIT clinical manifestations were the most reported symptoms. Forty percent of the children were admitted to the inpatient ward. Interestingly, 29.4% were discharged against medical advice. Approximately 43% showed complete recovery. The logistic regression model of predictors of accidental intoxication indicated that only age and residence in urban vs rural areas had a statistically significant relationship. Conclusions: Acute pediatric intoxication is a problem in Aljouf, KSA. Caregivers' awareness of the potentially hazardous toxic agents and risk factors for pediatric intoxication should be enhanced, and effective prevention strategies should be implemented to decrease the incidence of pediatric intoxication.

Alleviation of doxorubicin-induced cardiotoxicity in rat by mesenchymal stem cells and olive leaf extract via MAPK/ TNF-α pathway: Preclinical, experimental and bioinformatics enrichment study.

BACKGROUND: Toxic cardiomyopathies were a potentially fatal adverse effect of anthracycline therapy. AIM: This study was conducted to demonstrate the pathogenetic, morphologic, and toxicologic effects of doxorubicin on the heart and to investigate how the MAPK /TNF-α pathway can be modulated to improve doxorubicin-Induced cardiac lesions using bone marrow-derived mesenchymal stem cells (BM-MSCs) and olive leaf extract (OLE). METHODS: During the study, 40 adult male rats were used. Ten were used to donate MSCs, and the other 30 were split into 5 equal groups: Group I was the negative control, Group II obtained oral OLE, Group III obtained an intraperitoneal cumulative dose of DOX (12 mg/kg) in 6 equal doses of 2 mg/kg every 48 h for 12 days, Group IV obtained intraperitoneal DOX and oral OLE at the same time, and Group V obtained intraperitoneal DOX and BM-MSCs through the tail vein at the same time for 12 days. Four weeks after their last dose of DOX, the rats were euthanized. By checking the bioinformatic databases, a molecularly targeted path was selected. Then the histological, immunohistochemistry, and gene expression of ERK, JNK, NF-κB, IL-6, and TNF-α were done. RESULTS: Myocardial immunohistochemistry revealed severe fibrosis, cell degeneration, increased vimentin, and decreased CD-31 expression in the DOX-treated group, along with a marked shift in morphometric measurements, a disordered ultrastructure, and overexpression of inflammatory genes (ERK, NF-κB, IL-6, and TNF-α), oxidative stress markers, and cardiac biomarkers. Both groups IV and V displayed reduced cardiac fibrosis or inflammation, restoration of the microstructure and ultrastructure of the myocardium, downregulation of inflammatory genes, markers of oxidative stress, and cardiac biomarkers, a notable decline in vimentin, and an uptick in CD-31 expression. In contrast to group IV, group V showed a considerable beneficial effect. CONCLUSION: Both OLE and BM-MSCs showed an ameliorating effect in rat models of DOX-induced cardiotoxicity, with BM-MSCs showing a greater influence than OLE.

Platelet Rich Plasma and Adipose-Derived Mesenchymal Stem Cells Mitigate Methotrexate-Induced Nephrotoxicity in Rat via Nrf2/Pparγ/HO-1 and NF-Κb/Keap1/Caspase-3 Signaling Pathways: Oxidative Stress and Apoptosis Interplay.

BACKGROUND: the nephrotoxicity of methotrexate (MTX) is observed in high-dose therapy. Moreover, low-dose MTX therapy for rheumatic diseases is debatable and claimed to cause renal impairment. This study aimed at studying the effect of methotrexate in repeated low doses on rat kidneys and assessing the efficacy of adipose-derived mesenchymal stem cells (AD-MSCs) and platelet rich plasma (PRP) for attenuating this effect. METHODS: Forty-two male Wistar rats were used, 10 rats were donors of AD-MSCs and PRP, 8 rats served as control, and the remaining rats were subjected to induction of nephrotoxicity by MTX intraperitoneal injection once weekly for successive 8 weeks and then assigned into 3 groups of 8 animals each: Group II: received MTX only. Group III: received MTX + PRP. Group IV: received MTX + AD-MSCs. After one month, rats were anaesthetized, serum-sampled, and renal tissue removed for biochemical, histological, and ultrastructural evaluation. RESULTS: there was significant tubular degeneration, glomerulosclerosis, fibrosis, decreased renal index, along with increased levels of urea and creatinine in the MTX group compared to the control group. Immunohistochemical expression of caspase-3 and iNOS in the renal tissue was significantly increased in group II compared to groups III and IV. Biochemical results revealed higher tissue malondialdehyde (MDA) concentration in the MTX-injected group which decreased significantly in co-treatment with either AD-MSC or PRP + MTX. MSC promoted the activation of the Nrf2/PPARγ/HO-1 and NF-κB/Keap1/caspase-3 pathways, increased antioxidant enzyme activities, reduced lipid peroxidation levels, and alleviated oxidative damage and apoptosis. PRP showed therapeutic effects and molecular mechanisms similar to MSC. Furthermore, MSC and PRP treatment significantly reduced MTX-induced upregulation of the pro-inflammatory (NF-κB, interleukin-1ß, and TNF-α), oxidative stress (Nrf-2, hemoxygenase-1, glutathione, and malondialdehyde), and nitrosative stress (iNOS) markers in the kidney. CONCLUSION: repeated administration of low-dose MTX resulted in massive renal tissue toxicity and deterioration of renal function in rats which proved to be attenuated by PRP and AD-MSCs through their anti-inflammatory, anti-apoptotic and anti-fibrotic properties.

Urine-Derived Stem Cells Versus Their Lysate in Ameliorating Erectile Dysfunction in a Rat Model of Type 2 Diabetes.

Background: Diabetic erectile dysfunction (DED) is a significant consequence of diabetes mellitus, and it is a multifactorial phenomenon that has no definitive treatment until now. Many therapeutic options provide symptomatic improvement rather than addressing the underlying etiology or restoring normal function. Stem cell (SC) therapy represents a potential hope in DED management. It is well established that the regenerative effect of stem cells can be attained by their paracrine action and their ability to differentiate into many cell lineages, including endothelial and smooth muscle cells. Hence, we tried to compare the effects of transplantation of urine-derived stem cells (USCs) or their lysate (USC-L) into the corpora cavernosa (CCs) of rats with DED. Materials and Methods: A total of 55 adult male Wistar rats were included in this study. USCs were obtained from ten healthy rats. Another ten rats did not subject to any intervention and served as a control (group I). Type 2 DM and DED were induced in the remaining 35 rats, but DED was tested and proved in only 24 rats, which were randomly divided into three groups (n = 8 in each). The DED group (group II) and either USCs (2 × 106 cells) or their lysate (200 µl) were transplanted into the CCs of each rat in the other two groups (groups III and IV), respectively. Results: Although the DED rats exhibited deterioration in all copulatory functions as compared to the control group, our histopathological, immunohistochemical, and morphometric results revealed that both USCs and USC-L have significantly restored the cavernous spaces, the ultrastructures of the endothelium that line the cavernous spaces, collagen/smooth muscle ratio, and the mean area percentage of α-SMA in the CCs as compared to DED rats. A respectable number of USCs was detected in the CCs of group III at the 4th week after transplantation, but this number significantly declined by the 8th week. Conclusion: Both USCs and USC-L can repair the structure and ultrastructure of CCs and improve the copulatory functions in the DED rat model. However, USC-L could be better used in DED to guard against the strange behavior of USCs after transplantation and their decreased survivability with time.

Bone-Marrow-Derived Mesenchymal Stem Cells, Their Conditioned Media, and Olive Leaf Extract Protect against Cisplatin-Induced Toxicity by Alleviating Oxidative Stress, Inflammation, and Apoptosis in Rats.

BACKGROUND: Hepatic and renal damage is a cisplatin (Cis)-induced deleterious effect that is a major limiting factor in clinical chemotherapy. OBJECTIVES: The current study was designed to investigate the influence of pretreatment with olive leaf extract (OLE), bone-marrow-derived mesenchymal stem cells (BM-MSC), and their conditioned media (CM-MSC) against genotoxicity, nephrotoxicity, hepatotoxicity, and immunotoxicity induced by cisplatin in rats. METHODS: The rats were randomly divided into six groups (six rats each) as follows: Control; OLE group, treated with OLE; Cis group, treated with a single intraperitoneal dose of Cis (7 mg/kg bw); Cis + OLE group, treated with OLE and cisplatin; Cis + CM-MSC group, treated with BM-MSC conditioned media and Cis; and Cis + MSC group, treated with BM-MSC in addition to Cis. RESULTS: Cis resulted in a significant deterioration in hepatic and renal functions and histological structures. Furthermore, it increased inflammatory markers (TNF-α, IL-6, and IL-1ß) and malondialdehyde (MDA) levels and decreased glutathione (GSH) content, total antioxidant capacity (TAC), catalase (CAT), and superoxide dismutase (SOD) activity in hepatic and renal tissues. Furthermore, apoptosis was evident in rat tissues. A significant increase in serum 8-hydroxy-2-deoxyguanosine (8-OH-dG), nitric oxide (NO) and lactate dehydrogenase (LDH), and a decrease in lysozyme activity were detected in Cis-treated rats. OLE, CM-MSC, and BM-MSC have significantly ameliorated Cis-induced deterioration in hepatic and renal structure and function and improved oxidative stress and inflammatory markers, with preference to BM-MSC. Moreover, apoptosis was significantly inhibited, evident from the decreased expression of Bax and caspase-3 genes and upregulation of Bcl-2 proteins in protective groups as compared to Cis group. CONCLUSIONS: These findings indicate that BM-MSC, CM-MSC, and OLE have beneficial effects in ameliorating cisplatin-induced oxidative stress, inflammation, and apoptosis in the hepatotoxicity, nephrotoxicity, immunotoxicity, and genotoxicity in a rat model.

Evaluation of vitamin C protective effect on the cerebrocortical antioxidant defense, histopathological, pro-apoptotic p53 and anti-apoptotic Bcl2 expressions against tramadol neurotoxicity in rats.

BACKGROUND: Reported tramadol toxicity emphasizes the necessity to recognize its mechanism of toxicity, particularly to the brain tissue. AIM: This study aimed to evaluate the protective effect of vitamin C (Vit C) in cerebrocortical toxicity mediated by tramadol in rats using biochemical and histological parameters. MATERIAL AND METHODS: Forty-eight albino rats were randomly divided into eight groups, (n = 6/group) as follow: the control group received normal saline and vitamin C group received vitamin C (200 mg/kg per oral). Tramadol 50, 100, 150 groups received tramadol in doses of (50, 100 and 150 mg/kg per oral, respectively); Tramadol 50+ Vit C, 100+ Vit C, 150+ Vit C groups received vitamin C (200 mg/kg per oral) plus tramadol in doses of (50, 100 and 150 mg/kg per oral, respectively). Rats had received vitamin C and tramadol daily for 30 days. Blood and brain tissues samples were harvested for biochemical, histopathological, immunohistochemical and electron microscopic examinations. RESULTS: Tramadol administration leads to a significant elevation of MDA, NO levels and a significant decrease in antioxidants parameters (CAT, SOD and GSH) in the tissues of cerebral cortices in rats which were directly proportional to the dose of tramadol. In histological investigations, tramadol-treated groups showed pyknotic pyramidal cells, multiple red neurons and shrinking red neurons with hallows around it and apoptotic cells were detected. These biochemical abnormalities and histological impairment were ameliorated in groups with tramadol low doses by the co-treatment with vitamin C. CONCLUSION: vitamin C has antioxidant and anti-apoptotic potentials against tramadol neurotoxicity via suppression of oxidative stress, lipid peroxidation, structural abnormalities, and down-regulation of p53 and overexpression of Bcl2 in the nervous tissues.

Cardioprotective effect of green tea extract and vitamin E on Cisplatin-induced cardiotoxicity in mice: Toxicological, histological and immunohistochemical studies.

BACKGROUND: Cisplatin (CP) has been used in wide range for cancer treatment. Although nephrotoxicity of CP was the main complication, cardiotoxicity has been reported. OBJECTIVES: This study investigates the protective role of green tea extract (GTE) and vitamin E (Vit-E) against CP-induced cardiotoxicity, and assesses their impact on CP antitumor efficacy. MATERIALS AND METHODS: Forty-eight male albino Balb/c mice were randomly divided into six groups, 8 per/group (Gp) were included. Gp1 served as control; Gp2 and Gp3 received oral GTE (400 mg/kg) and Vit-E (100 mg/kg) for 30 consecutive days respectively. Gp4 had received CP (7 mg/kg i.p.) once on the 27th day; Gp5 had received GTE (400 mg/kg p.o.) for 30 days and CP (7 mg/kg i.p.) on the 27th day. Gp6 had received Vit-E (100 mg/kg p.o.) for 30 days and CP (7 mg/kg i.p.) on the 27th day. Blood and tissues samples were harvested for biochemical and histopathological investigations. To evaluate the effect of GTE and Vit-E on the antitumor efficacy of CP, 49 female albino mice were inoculated intraperitoneally by Ehrlich ascetic carcinoma -cells (2 × 106/mouse) then treated with none, corn oil, CP, CP/GTE, CP/Vit-E, GTE or Vit-E. RESULTS: CP injection significantly increased Troponin I, CPK, CK-MB, malondialdehyde (MDA), and nitric oxide (NO) levels, while glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase levels were significantly reduced with disruption of cardiac muscle fibers, loss of striations, absence of intercalated disc, and the nuclei are pyknotic. Treatment with GTE and Vit-E improve the biochemical and histological parameters. Treatment with CP alone led to eradication of the tumor cells from the tumor-bearing mice. However, co-administration of GTE or Vit-E orally with CP did not interfere with its therapeutic effects. CONCLUSION: Treatment with GTE and Vit-E significantly ameliorated the CP cardiotoxicity and improved the myocardial histopathological architecture. GTE and Vit-E may be combined with CP to alleviate cardiotoxicity in cancer chemotherapy without interfering with its antitumor activity.

Histopathological differentiation of drowning in freshwater and saltwater in rats: forensic point of view / Diferenciación histopatológica de ahogamiento en agua dulce y agua salada en ratas: punto de vista forense

SUMMARY: The postmortem diagnosis of death by drowning is one of the most difficult issues in forensic pathology. We investigated possible evidence differentiating saltwater drowning from freshwater drowning by histopathological changes in brain, heart, lungs, liver, and kidneys tissues. A cross section descriptive study was carried out on eighteen 12-week-old male Wistar rats; they were divided equally into 3 groups. Group 1: control group; Group 2: death by drowning in freshwater; Group 3: death by drowning in saltwater. Immediately after death, all tested organs were removed and fixed for histopathological examination. The brain of freshwater group depicted degenerated neurocytes with dystrophic changes in the form of shrunken cell, pyknotic nuclei and deeply eosinophilic cytoplasm. The heart showed clear evidence of myocyte injuries in saltwater drowning compared to the control and freshwater groups. The kidneys of rats drown in saltwater revealed more glomerular destruction with no differences in tubulo-interstitial changes in comparison with those drown in freshwater. In the lungs, the changes in freshwater were restricted to the alveoli, and the bronchial changes were more distinctive in saltwater. No disturbed liver architecture was seen in both test groups, however hydropic degeneration, congested vessels, and sinusoids were more distinct in saltwater group. In conclusion, diagnostic differentiation between fresh and saltwater drowning was reliable in rats' lungs and heart with minimal differentiation in liver, kidneys, and brain. Further studies of drowning with different staining techniques will help to clarify the potential role of histopathological changes in body organs as indicator of drowning.

RESUMEN: El diagnóstico post mortem de muerte por ahogamiento es uno de los temas más difíciles de la patología forense. Investigamos la posible evidencia que diferencia el ahogamiento en agua salada del ahogamiento en agua dulce por cambios histopatológicos en los tejidos del cerebro, el corazón, los pulmones, el hígado y los riñones. Se realizó un estudio descriptivo de corte transversal en dieciocho ratas Wistar macho de 12 semanas de edad; se dividieron por igual en 3 grupos. Grupo 1: grupo control; Grupo 2: muerte por ahogamiento en agua dulce; Grupo 3: muerte por ahogamiento en agua salada. Inmediatamente después de la muerte, se extirparon todos los órganos analizados y se fijaron para el examen histopatológico. El cerebro del grupo de agua dulce mostró neurocitos degenerados con cambios distróficos en forma de células encogidas, núcleos picnóticos y citoplasma profundamente eosinofílico. El corazón mostró una clara evidencia de lesiones de miocitos en los ahogamientos en agua salada en comparación con los grupos de control y de agua dulce. Los riñones de ratas ahogadas en agua salada revelaron una mayor destrucción glomerular sin diferencias en los cambios túbulo-intersticiales en comparación con las ahogadas en agua dulce. En los pulmones, los cambios en agua dulce se restringieron a los alvéolos y los cambios bronquiales fueron más distintivos en agua salada. No se observó una arquitectura hepática alterada en ambos grupos de prueba, sin embargo, la degeneración hidrópica, los vasos congestionados y los sinusoides fueron más distintos en el grupo de agua salada. En conclusión, la diferenciación diagnóstica entre ahogamiento en agua dulce y salada fue confiable en los pulmones y el corazón de las ratas con una diferenciación mínima en el hígado, los riñones y el cerebro. Estudios adicionales de ahogamiento con diferentes técnicas de tinción ayudarán a aclarar el papel potencial de los cambios histopatológicos en los órganos del cuerpo como indicador de ahogamiento.

Assessment of the Toxicity of Sub-chronic Low and High Doses of the Bio-insecticide Spinosad on the Liver, Kidney and the Cerebellum in Male Albino Mice

ABSTRACT Spinosad (SPD) is a highly selective insect control product. However, it was reported that SPD has toxicity toward other non-target organisms. This study was conducted to address the toxic effect of two sub-chronic low and high doses; 35 and 350 mg/kg SPD on some biochemical, histological and immunohistochemical parameters of the liver, kidney and cerebellum. Thirty-six male Swiss mice were divided into three groups of 12 mice each; first group (G1) served as a control, second group (G2) received a low sub-chronic dose of SPD that is equal to 35 mg/kg, and third group (G3) received a high sub-chronic dose of SPD that is equal to 350 mg/kg. The results showed that mice which were received 350 mg/kg SPD showed a significant decrease in the body weight and a significant increase in their relative kidney and spleen weights. They also showed a significant increase in alanine aminotransferase (ALT), triglycerides and urea levels. Histopathological examination showed cytoplasmic degeneration and cell necrosis in the liver and kidney. Immunohistochemical examination showed that cerebellum illustrated several neurodegenerative changes and a down-regulation of synaptophysin-Syp. In conclusion, exposure to a high dose of SPD that is equal to 350 mg/kg could cause a marked toxicity on the liver, kidney and cerebellum in male albino mice.