Destructive Adsorption of Diazinon Pesticide by Activated Carbon Nanofibers Containing Al2O3 and MgO Nanoparticles

We report the destructive adsorption of Diazinon pesticide by porous webs of activated carbon nanofibers containing Al₂O₃ and MgO nanoparticles. The results show that, the presence of Al₂O₃ and MgO nanoparticles in the activated carbon nanofibers increases the amount of destructively adsorbed Diazinon pesticide by activated carbon nanofibers. Moreover, type, amount, and specific surface area of metal oxide nanoparticles affect the adsorption rate as well as the total destructively adsorbed Diazinon. Liquid chromatography proved the degradation of Diazinon by chemical reaction with Al₂O₃ and MgO nanoparticles. Liquid chromatography–mass spectrometry showed that the main product of reaction between Diazinon and the metal oxides is 2-isopropyl-6-methyl-4-pyrimidinol with less toxicity than Diazinon.     

Tissue factor antisense deoxyoligonucleotide prevents monocrotaline/LPS hepatotoxicity in mice

Tissue factor (TF) is a membranous glycoprotein that functions as a receptor for coagulation factor VII/VIIa and activates the coagulation system when blood vessels or tissues are damaged. TF was upregulated in our monocrotaline (MCT)/lipopolysaccharide (LPS) hepatotoxicity model. We tested the hypothesis that TF‐dependent fibrin deposition and lipid peroxidation in the form of oxidized low‐density‐lipoprotein (ox‐LDL) accumulation contribute to liver inflammation induced by MCT/LPS in mice. In the present study, we blocked TF using antisense oligodeoxynucleotides against mouse TF (TF‐ASO). TF‐ASO (5.6 mg kg^?1) was given i.v. to ND4 male mice 30 min after administration of MCT (200 mg kg^?1) p.o. followed after 3.5 h by LPS i.p. (6 mg kg^?1). Blood alanine aminotransferase (ALT), TF, ox‐LDL, platelets, hematocrit and keratinocyte‐derived chemokine (KC) levels were evaluated in different treatment groups. Fibrin deposition and ox‐LDL accumulation were also analyzed in the liver sections using immunofluorescent staining. The results showed that TF‐ASO significantly restored blood ALT, hematocrit and KC levels, distorted after MCT/LPS co‐treatment, as well as preventing the accumulation of ox‐LDL and the deposition of fibrin in the liver tissues, and thereby inhibited liver injury caused by MCT/LPS. In a separate experiment, TF‐ASO administration significantly prolonged animal survival. The current study demonstrates that TF is associated with MCT/LPS‐induced liver injury. Administration of TF‐ASO successfully prevented this type of liver injury. Copyright © 2012 John Wiley & Sons, Ltd.     

MRI as complementary tool added to ultrasound in the diagnosis of fetal renal abnormalities – any added value?

Purpose

To assess the potential role of magnetic resonance imaging (MRI) as a complementary diagnostic tool to ultrasonography (US) in the diagnosis of fetal renal anomalies in pregnant women with oligohydramnios in the absence of amniotic membrane rupture.

Methods

Ninety pregnant women, with oligohydramnios were prospectively evaluated using both US and MRI. Prenatal findings were correlated with the babies’ outcome.

Results

MRI studies of diagnostic quality were obtained in all fetuses. The US and MRI findings were concordant in 79 (87.8%) of the fetuses. MRI modified and changed the diagnosis in 11 fetuses (12.2%), these were five fetuses in which US diagnosis was inconclusive, five cases in which the diagnosis changed from bilateral renal agenesis to unilateral agenesis with the other kidney multicystic dysplastic kidney (MCDK), and in the remaining fetuses the modification was from bilateral renal agenesis to unilateral agenesis with the other kidney structurally normal.Concordant findings for the prenatal US and MRI scans were seen in 100% of the autosomal recessive polycystic kidney disease (APCKD), 96% of MCDK, and 92.9% of bilateral normal kidneys.

Conclusion

MRI is of value in cases of oligohydramnios in limited circumstance when US findings were inconclusive.     

GSTP1, GSTM1, and GSTT1 genetic polymorphisms in patients with cryptogenic liver cirrhosis

We investigated glutathione S-transferase (GST) P1I le (105) Val, T1, and M1 polymorphisms in 45 patients with documented cryptogenic cirrhosis and 56 healthy control subjects. Polymerase chain reaction-based procedures were performed in the studied populations to confirm the genotypes of GSTT1, M1, and P1. Ile/Val and Val/Val GSTP1 genotypes were more frequent in the patients with cirrhosis (n = 39, 87%) than in the control subjects (n = 10; 18%) (odds ratio [OR] 34.04; 95% confidence interval [CI] 10.70 to 108.31, P < 0.001). Among these patients with cirrhosis, 16 were heterozygous and 23 were homozygous, whereas only one person in the control group was homozygous. The GSTM1 null genotype was also more prevalent in cirrhotic patients than in healthy control subjects (OR 6.83, 95% CI 2.53 to 18.42, P < 0.001). The rate of GSTT1 deletion did not show a significant difference between the two groups (OR 2.35, 95% CI 0.76 to 7.28, P = 0.111). To our knowledge, this is the first evidence that GSTP1 and GSTM1 polymorphisms may be related to the development of cirrhosis by unknown mechanisms. The significant association of cryptogenic cirrhosis with Val/Val GSTP1 genotype encoding a low detoxification activity protein implicates this polymorphism as a risk factor for the occurrence of the disease. Presented as an abstract at the Forty-Fourth Annual Meeting of The Society for Surgery of the Alimentary Tract, Orlando, Florida, May 19–22, 2003 (Poster of Distinction).     

A Psychometric Indices of the Farsi Version of the Believability of Anxious Feelings and Thoughts Questionnaire (BAFT)

The following paper aimed to adapt and validate the Farsi version of the Believability of Anxious Feelings and Thoughts Questionnaire (BAFT), which measures cognitive fusion/defusion, one of the six components in Acceptance and Commitment Therapy (ACT). The authors assessed the psychometric properties of the BAFT in a sample of undergraduate students. Exploratory Factor Analysis supported a three-factor structure with 16 items. The results from a Confirmatory Factor Analysis showed the goodness of fit of the model. The test also demonstrated a good level of internal consistency and incremental validity. Overall, the results show that the Farsi version of BAFT is a consistent and valid scale.     

Screening for vesicoureteral reflux and renal scars in siblings of children with known reflux

The incidence of vesicoureteral reflux (VUR) in the general population is less than 1%, but it is high in families with reflux. The reported prevalence of VUR among siblings of index patients with reflux has ranged from 4.7% to 51%. Reflux carries an increased risk of pyelonephritis and long-term renal impairment. The purpose of this study was to identify the age-related incidence and severity of reflux, and the frequency of associated renal parenchymal damage in siblings of children with reflux in order to assess the use of screening at different ages. Between October 1994 and February 2003, 40 siblings of 34 index patients were screened with direct voiding cystography. 99( m ) technetium (Tc)-dimercaptosuccinic acid (DMSA) nuclear renal scans were performed in siblings with VUR to detect renal scarring. The cystograms were interpreted as showing the presence or absence of VUR and the DMSA scan as symmetrical or asymmetrical differential function, with or without renal scarring. Of 40 siblings, 17 had VUR, representing an incidence of 42.5%. The mean age at study entry of the 15 boys and 25 girls was 63 months (range 6 months to 12 years). The majority of siblings with abnormal DMSA scans were asymptomatic. Reflux was unilateral in 12 siblings and bilateral in 5. Of the 17 refluxing siblings (22 refluxing ureters), 7 (41.17%) had a history of symptomatic urinary tract infection (UTI). The frequency of VUR was nearly equal in siblings over 6 years and those younger than 6 years. Of the 17 siblings with VUR, 16 had DMSA scintigraphy. Of these, 5 were normal and 11 (68.75%) showed abnormalities (7 asymmetrical differential function and 4 parenchymal defect), which was bilateral in 7 and unilateral in 4. In conclusion, this study confirms a significant overall incidence of VUR and renal parenchymal damage in the siblings of patients with known reflux. The prevalence of reflux in older siblings is similar to that in younger siblings. Our review suggests that all siblings over 6 years should undergo a screening cystogram, even in the absence of urinary tract infection. DMSA scintigraphy of asymptomatic siblings appears to be beneficial in preventing renal injury.     

Identification of the phrenic nerve in surgical exploration of the brachial plexus in obstetrical palsy

This report describes a simple technique for identifying the phrenic nerve at the beginning of exploration of the brachial plexus in obstetrical palsy. Both the phrenic and supraclavicular nerves originate from the C4 root; therefore, retrograde dissection of the supraclavicular nerve will end at the C4 root and identify the phrenic nerve. This technique is very useful to less experienced surgeons but may also be helpful when the experienced surgeon encounters excessive scarring of the anterior scalene muscle. Finally, the dissected supraclavicular nerve may be used as a cable graft in brachial plexus reconstruction.     

A Comparison of Classical and Anatomical Total Knee Alignment Methods in Robotic Total Knee Arthroplasty : Classical and Anatomical Knee Alignment Methods in TKA

The purpose of this study was to compare the clinical and radiological outcomes achieved using classical and anatomical alignment methods in primary total knee arthroplasty (TKA). One hundred and seventeen patients were randomly assigned to undergo robotic-assisted TKA using either the classical (56 patients) or the anatomical alignment method (61 patients). Clinical outcomes including varus and valgus laxities, ROM, HSS and WOMAC scores and radiological outcomes were evaluated after a minimum follow-up of 2 years. Varus and valgus laxity assessments showed no significant inter-group differences (P > 0.05). Moreover, no significant differences were observed in ROM, HSS and WOMAC scores (P > 0.05). We could not find any significant difference in mechanical alignment of the lower limb. The results of this study show that two alignment methods provide comparable clinical and radiological outcomes after primary TKA.     

Hyperactive Transforming Growth Factor‐β1 Signaling Potentiates Skeletal Defects in a Neurofibromatosis Type 1 Mouse Model

Dysregulated transforming growth factor beta (TGF‐β) signaling is associated with a spectrum of osseous defects as seen in Loeys‐Dietz syndrome, Marfan syndrome, and Camurati‐Engelmann disease. Intriguingly, neurofibromatosis type 1 (NF1) patients exhibit many of these characteristic skeletal features, including kyphoscoliosis, osteoporosis, tibial dysplasia, and pseudarthrosis; however, the molecular mechanisms mediating these phenotypes remain unclear. Here, we provide genetic and pharmacologic evidence that hyperactive TGF‐β1 signaling pivotally underpins osseous defects in Nf1^flox/?;Col2.3Cre mice, a model which closely recapitulates the skeletal abnormalities found in the human disease. Compared to controls, we show that serum TGF‐β1 levels are fivefold to sixfold increased both in Nf1^flox/?;Col2.3Cre mice and in a cohort of NF1 patients. Nf1‐deficient osteoblasts, the principal source of TGF‐β1 in bone, overexpress TGF‐β1 in a gene dosage–dependent fashion. Moreover, Nf1‐deficient osteoblasts and osteoclasts are hyperresponsive to TGF‐β1 stimulation, potentiating osteoclast bone resorptive activity while inhibiting osteoblast differentiation. These cellular phenotypes are further accompanied by p21‐Ras–dependent hyperactivation of the canonical TGF‐β1–Smad pathway. Reexpression of the human, full‐length neurofibromin guanosine triphosphatase (GTPase)‐activating protein (GAP)‐related domain (NF1 GRD) in primary Nf1‐deficient osteoblast progenitors, attenuated TGF‐β1 expression levels and reduced Smad phosphorylation in response to TGF‐β1 stimulation. As an in vivo proof of principle, we demonstrate that administration of the TGF‐β receptor 1 (TβRI) kinase inhibitor, SD‐208, can rescue bone mass deficits and prevent tibial fracture nonunion in Nf1^flox/?;Col2.3Cre mice. In sum, these data demonstrate a pivotal role for hyperactive TGF‐β1 signaling in the pathogenesis of NF1‐associated osteoporosis and pseudarthrosis, thus implicating the TGF‐β signaling pathway as a potential therapeutic target in the treatment of NF1 osseous defects that are refractory to current therapies. © 2013 American Society for Bone and Mineral Research.