Evaluation of faecal lactoferrin as a morbidity biomarker in Schistosoma mansoni infection.

OBJECTIVE: Lactoferrin is an 80 KDa iron-binding glycoprotein that plays a significant role in the innate immune system and is considered to be an important microbicide molecule. This study aimed to assess the concentration of lactoferrin in Schistosoma mansoni-infected cases before and after praziquantel treatment. METHODS: A cross-sectional study was carried out on 250 individuals aged from 5 to 30 years. Stool samples were examined for the presence of parasitic infections using Kato-Katz and formalin ethyl acetate techniques. All S. mansoni-positive cases were treated with praziquantel and stool samples were recollected 21 days later. Faecal lactoferrin level was determined before and after treatment. RESULTS: The prevalence of S. mansoni infection was 14.4%. Among 36 participants infected with S. mansoni, the cure rate was 91.7%. A statistically significant difference in the mean lactoferrin level before and after treatment was detected (1648.95 pg/ml ± 656.5 vs. 1162.8 pg/ml ± 356.8). This difference was statistically significant in the middle and older age groups, in males and in the absence of coinfection with other parasites. CONCLUSION: Lactoferrin could be a promising biomarker associated with S. mansoni infection, however, it could not be used to assess the severity of infection.

Chlorella vulgaris ameliorates sodium nitrite-induced hepatotoxicity in rats.

The current was conducted to evaluate the ameliorating effect of Chlorella vulgaris (CV) extract against sodium nitrite-induced hepatotoxicity in rats. Forty-five rats were allocated randomly into 5 groups (n = 9). Group I (GI), control group: orally gavaged with normal saline daily. Group II (GII): orally gavaged with CV extract (70 mg/kg BW) for 3 months. Group III (GIII): orally gavaged with sodium nitrite (80 mg/kg BW) for 3 months. Group IV (GIV): received sodium nitrite as GIII and CV extract as GII simultaneously for 3 months. Group V (GV): received CV extract as GII and then, sodium nitrite as in GIII from the end of first month until the end of the experiment. Sodium nitrite significantly increased the activities of serum alanine aminotransferase, aspartate aminotransferase, and serum concentrations of tumor interleukin 1-ß and necrosis factor α. In addition, it increased concentrations of malondialdehyde and nitric oxide and expression level of caspase-3 in the hepatic tissue. However, it decreased activities of hepatic glutathione peroxidase, catalase, and superoxide dismutase and induced degenerative and necrotic changes in hepatic tissues. In contrast, CV extract administration modulated sodium nitrite-induced inflammation, oxidative stress, and alteration in hepatic tissue function and architecture. This study indicated that CV extract modulated sodium nitrite-induced hepatic toxicity through decreasing oxidative stress and inflammation and enhancing antioxidant enzyme activities in hepatic tissue of rats.

Validation of electrical velocimetry in resuscitation of patients undergoing liver transplantation. Observational study.

Major hemodynamic changes are frequently noted during liver transplantation (LT). We evaluated the performance of electrical velocimetry (EV) as compared to that of TEE in SV optimization during liver transplantation. This was an observational study in 32 patients undergoing LT. We compared SV values measured simultaneously by EV (SVEV) and TEE (SVTEE) at baseline 30 min after induction, at the end of dissection phase, 30 min after anhepatic phase, 30 min after reperfusion. We also evaluated the reliability of EV to track changes In SV before and after 49 fluid challenges. Finally, the SV variation (SVV) and pulse pressure variation (PPV) were tested as predictors for volume responsiveness, defined as an increase in SV ≥ 10% after 250 ml of colloid. For 112 paired SV data, the overall correlation was 0.76 and bias (limits of agreement) 0.3 (- 29 to 29) ml percentage error 62%. The EV was able to track changes in SV with a concordance rate of 97%, and a sensitivity and specificity of 93% to detect a positive fluid challenge. The AUC values (with 95% confidence intervals) for SVV and PPV were 0.68 (0.52-0.83) and 0.72 (0.57-0.86), respectively, indicating low predictive capacity in these setting. The absolute values of SV derived from EV did not agree with SV derived from TEE. However, EV was able to track the direction of changes in SV during hemodynamic management of patients undergoing liver transplantation.Clinical trial registration: Clinicaltrials.gov Identifier: NCT03228329 prospectively Registered on 13-July-2017.

Ameliorative effect of pumpkin seed oil against emamectin induced toxicity in mice.

The current study was conducted to evaluate the toxic effects of emamectin insecticide in mice and the possible protective effect of pumpkin seed oil. Treated mice received emamectin benzoate in the diet at 75-ppm for 8 weeks, while another group of animals received emamectin in addition to pumpkin seed oil at a dose of 4 ml/kg. Biochemical analysis of MDA, DNA fragmentation, GSH, CAT and SOD was performed in liver, kidney and brain as oxidant/antioxidant biomarkers. In addition, gene expression of CYP2E1 and Mgst1 and histopathological alterations in these organs were evaluated. Emamectin administration induced oxidative stress in liver and kidney evidenced by elevated levels of MDA and percentage of DNA fragmentation with suppression of GSH level and CAT and SOD activities. Brain showed increase of MDA level with inhibition of SOD activity. Relative expressions of CYP2E1 and Mgst1 genes were significantly elevated in both liver and kidney. Emamectin produced several histopathological changes in liver, kidney and brain. Co-administration of pumpkin seed oil produced considerable protection of liver and kidney and complete protection of brain. In conclusion, pumpkin seed oil has valuable value in ameliorating the toxic insult produced by emamectin in mice.

Clinical, pathological, and molecular data concerning Coenurus cerebralis in Sheep in Egypt.

This article contains information related to a recent study "Prevalence and Identity of Taenia multiceps cysts "Coenurus cerebralis" in Sheep in Egypt" (Amer et al., 2017) [1]. Specifically, affected sheep showed neurological disorders manifested as depression, head shaking and circling, altered head position, incoordination and paralysis in some cases. Brain-derived cysts were molecularly identified by PCR-sequence analysis at mitochondrial 12S rRNA gene marker. Cyst-induced pathological changes included degenerative changes and demyelination in brain tissue, infiltration of lymphocytes and histiocytes. Cystic fluids were biochemically analyzed for protein, lipids and electrolytes. The data of this study provides more understanding on phylogeny, epidemiology and pathology of coenurosis in sheep.

Prevalence and Identity of Taenia multiceps cysts "Coenurus cerebralis" in Sheep in Egypt.

Coenurosis is a parasitic disease caused by the larval stage (Coenurus cerebralis) of the canids cestode Taenia multiceps. C. cerebralis particularly infects sheep and goats, and pose a public health concerns. The present study aimed to determine the occurrence and molecular identity of C. cerebralis infecting sheep in Egypt. Infection rate was determined by postmortem inspection of heads of the cases that showed neurological manifestations. Species identification and genetic diversity were analyzed based on PCR-sequence analysis of nuclear ITS1 and mitochondrial cytochrome oxidase (COI) and nicotinamide adenine dinucleotide dehydrogenase (ND1) gene markers. Out of 3668 animals distributed in 50 herds at localities of Ashmoun and El Sadat cities, El Menoufia Province, Egypt, 420 (11.45%) sheep showed neurological disorders. Postmortem examination of these animals after slaughter at local abattoirs indicated to occurrence of C. cerebralis cysts in the brain of 111 out of 420 (26.4%), with overall infection rate 3.03% of the involved sheep population. Molecular analysis of representative samples of coenuri at ITS1 gene marker showed extensive intra- and inter-sequence diversity due to deletions/insertions in the microsatellite regions. On contrast to the nuclear gene marker, considerably low genetic diversity was seen in the analyzed mitochondrial gene markers. Phylogenetic analysis based on COI and ND1 gene sequences indicated that the generated sequences in the present study and the reference sequences in the database clustered in 4 haplogroups, with more or less similar topologies. Clustering pattern of the phylogenetic tree showed no effect for the geographic location or the host species.

Sequential protocol biopsies from renal transplant recipients show an increasing expression of active TGF beta.

Chronic allograft nephropathy (CAN) is a major cause of graft loss after renal transplantation. Implicated in the pathogenesis of this complication is overproduction of the cytokine transforming growth factor beta (TGF beta). In this study we measured changes in CAN's expression in stable patients early after transplantation, and studied links with established risk factors for CAN, such as delayed graft function, acute rejection, and cyclosporine exposure. We took biopsies from 40 renal allografts at time of transplantation (pre-perfusion), and then, using ultrasound guidance, at 1 week and 6 months after transplantation. An immunofluorescence technique was used to stain sections for active TGF beta. These were then assessed by semi-quantitative scanning laser confocal microscopy. There was very little variation in active TGF-beta expression among patients in their pre-perfusion biopsies. Expression had increased by 1 week and then very significantly by 6 months ( P<0.0001). Patients who suffered delayed graft function had increased TGF-beta expression at both time points. There was no difference regarding donor type, acute rejection, and immunosuppressive drug (cyclosporine or tacrolimus). There was no correlation between the amount of TGF-beta expression at any time-point and isotope glomerular filtration rate (GFR) at 12 months. This study demonstrated that in a group of stable renal allograft recipients, TGF-beta expression in the kidney increased after transplantation. As the study used protocol biopsies, this increase is unlikely to be due to acute events, and probably represents a genuine increase.