Caveolin 3 gene and mitochondrial tRNA methionin gene in Duchenne muscular dystrophy

It was recently reported that Duchene muscular dystrophy [DMD] patients and mdx mice have elevated levels of caveolin-3 expression in their skeletal muscles. However, it remains unknown whether this increased caveolin-3 levels contribute to the pathogenesis of DMD. Also mitochondrial DNA mutation in the tRNA methionin [tRNA Met] gene has been shown to be associated with muscle weakness, severe exercise intolerance, lactic acidosis and growth retardation. Since DMD is X-linked maternally inherited disease, mitochondrial mutation in tRNA [Met] gene can be suspected to be the cause for the inefficient splicing of dystrophin gene during its expression and can be implicated as the cause of dystrophin inactive protein. The aim of the present study is to investigate whether mutations in caveolin gene leads to its increased expression and/or mutation in the tRNA [Met] gene can be associated with DMD pathogenesis. Expression of caveolin mRNA by RT-PCR and mutations in caveolin gene and tRNA [Met] gene were measured in 28 patients presented with DMD symptoms using the single strand conformation polymorphism assay [SSCP]. Results gave further proof to decreased expression of inducible nitric oxide synthase [iNOS] mRNA, which leads to increased expression in caveolin 3 mRNA in lymphocytes of DMD patients compared to controls. However using SSCP, there was no evidence for tRNA [Met] gene mutation among DMD patients and only one patient presented a mutation in the caveolin gene compared to controls. There is an inverse relation between iNOS and Caveolin 3 in lymphocytes of DMD patients compared to controls. However, Caveolin 3 gene mutation is excluded as the main cause of increased caveolin gene expression. Also, there was no evidence for tRNA [Met] gene mutation among DMD patients

CD[95] as an early and sensitive marker of neonatal sepsis and disease outcome

This study was carried out on 33 neonates. They were classified into 2 groups: the first group included 18 septic neonates [9 males and 9 females] of these 11 were fullterm and 7 were perterm. The second group included 15 healthy neonates as a control group [7 males and 8 females] of these 10 were full term and 5 were preterm. All cases and controls were subjected to thorough history, clinical examination, laboratory investigation for both groups included: complete blood picture, total and differential leucocytic count, erythrocyte sedimentation rate [ESR], c-reactive protein [CRP], blood culture in septic cases and Fas /Apo 1 / CD[95]. The level of CD[95] is significantly elevated in septic full term and septic preterm compared to normal full term and normal preterm respectively [both P<0.0001]. Comparing CD[95] levels in septic neonates according to the severity of infection there was significant difference between cases who recovered and those who died [P<0.05]. There was no significant correlation between the levels of CD[95] in septic cases and the causative organism. Comparing CD[95] with other laboratory results, there was significant negative correlation between CD[95] levels and platelet count, significant positive correlation with total leucocytic count in septic full term and negative correlation in septic premature. There was also positive correlation between CD[95] level and CRP. In conclusion, soluble CD[95] can be used as an early and sensitive marker in diagnosis of neonatal sepsis

Evaluation of gentamicin - induced nephrotoxicity in rats treated with low doses of ibuprofen and diclofenac sodium

The purpose of the present investigation was to examine the effects of two nonsteroidal anti-inflammatory drugs [NSAIDs], ibuprofen [20 mg/kg/day] and diclofenac sodium [2.5 mg/kg/day], on the severity of gentamicin - induced nephrotoxicity in rats. Administration of gentamicin [100 mg/kg/day] for 5 days resulted in a significant elevation in renal cortical total phospholipids accompanied by a significant decrease in cortical Na[ +/- ] K[ +/- ] adenosine triphosphatase [ATPase] activity [P<0.01]. These changes were associated with significant decrease in body weight and increase in kidney weight. Serum creatinine and urea nitrogen were also elevated in all gentamicin treated rats [P<0.01]. In rats treated simultaneously with both gentamicin and either ibuprofen or diclefenac sodium for 5 days, all the measured parameters of renal dysfunction were similar in magnitude to those observed in rats treated with gentamicin alone. In contrast, rats treated with either ibuprofen or diclofenac sodium for 27 days and injected concurrently with gentamicin during the last 5 days of the treatment period had significantly greater kidney weight, lower renal cortical Na[ +/- ]K[ +/- ] ATPase activity and higher cortical phospholipid content, serum creatinine and urea nitrogen than did rats treated with gentamicin alone [P<0.05]. A 27 -day treatment with ibuprofen or diclofenac sodium alone resulted in no change in renal function. These results demonstrate that gentamicin nephrotoxicity was potentiated after the long [27 days] but not after the short [5 days] period of treatment with ibuprofen and diclofenac sodium. Thus, prolonged administration of NSAIDs even in therapeutic doses should be considered as a risk/actor that may increase the nephrotoxic potential of gentamicin

Enzyme immuno-assay for the detection of urine antibodies in children infected with schistosoma hematobium

Enzyme linked Immunosorbant assay [ELISA] and dot- ELISA were performed to detect antibodies to Schisosoma haematobium egg antigens [Sh-SEA] in midday urine samples obtained from parasitological by proven urinary schistosomiases infected children. The assays failed to capture specific antibodies in 25-30 percent of patient's urine samples. Enzyme immunoblot assay [EIB] revealed consistent recognition by all the urine samples from S. haematobium cases to 20-106 KDa antigenic bands of Sh-SEA. The use of urine samples from mansoniasis or normal individuals [n=23] indicated 87 percent diagnostic specificity of this EIB. Thus, immunoreactivity of urine to electrophoresed Sh-SEA antigen is highly sensitive and non-invasive technique that could be asuitable alternative to serum ELISA for diagnosis of haematobia, particularly, for epidemiological studies on children