Suppressive effect of Spirulina fusiformis on diclofenac-induced hepato-renal injury and gastrointestinal ulcer in Wistar albino rats: A biochemical and histological approach.

CONTEXT: The non-steroidal anti-inflammatory drug (NSAID), diclofenac causes hepato-renal toxicity and gastric ulcer. The aim of this study was to investigate the protective effect of Spirulina fusiformis on Diclofenac-induced toxicity in Wistar albino rats. METHODS: Rats were treated as follows: normal control (group I); diclofenac (50mg/kgb.w., i.p.) treated rats (group II); diclofenac-induced (50mg/kgb.w., i.p.) rats treated with Spirulina fusiformis (400mg/kgb.w., p.o.) (group III); diclofenac-induced (50mg/kgb.w., i.p.) rats treated with silymarin (25mg/kgb.w., p.o.) (group IV); Spirulina fusiformis (400mg/kgb.w., p.o.) alone treated rats (groupV). Biochemical (liver and kidney functional markers) and antioxidant parameters (enzymic and non-enzymic antioxidants) were measured in the blood and tissue homogenates of the rats. Evaluation of intestinal ulcer score and assessment of liver and kidney histology were also done. DISCUSSION: Alterations in the levels of biochemical and antioxidant assays and histopathological changes in liver and kidney proved the toxic effect of diclofenac. The ulcer score was significantly increased in the diclofenac treated rats. Spirulina fusiformis showed to reduce such changes and was able to restore normal antioxidant status in the rats. CONCLUSION: Our study proves the hepato-renal and gastroprotective activity of Spirulina fusiformis in diclofenac-treated rats.

A de novo interstitial deletion of chromosome 15 band q25 as revealed by FISH-technique.

We report a new chromosomal finding in a 20 month-old girl. The minor clinical features included: moderate mental retardation, microcephaly, mild hypotonia and hypertelorism. Initially, what appeared to be a terminal deletion of the long arm of one chromosome 15 [15q26-->qter] was determined to be an interstitial deletion involving band 15q25 as revealed by FISH-technique, showing the presence of intact telomeric hybridization signals. The cytogenetic diagnosis was thus modified to 46,XX, del (15) (pter-->q24::q26--> qter). Nevertheless, the function of the enzyme telomerase should not be ignored, as healing could occur following such terminal deletions. Consequently, it will remain a difficult task to distinguish terminal deletions from those that are interstitial.

Two Prader-Willi/Angelman syndrome loci present in an isodicentric marker chromosome.

We found an abnormal 47,XX,+mar karyotype in a patient with developmental delay, hypotonia, microcephaly, failure to thrive, and cognitive delay. When metaphases were hybridized with Prader-Willi and Angelman loci-specific probes by the FISH technique, two sites were noted at opposite positions on the marker chromosome. The alphoid satellite DNA probe documented the isodicentric nature while retention of the p arms on both sides of the marker chromosome was demonstrated by beta satellite probe. The patient does not exhibit manifestations of either syndrome despite the presence of these loci in tetrasomic dose. The present investigation suggests that other marker chromosomes be reevaluated, as their clinical manifestations are quite variable.

Ring chromosome 17 in a mentally retarded boy.

A six-year-old boy was found to have a ring chromosome 17. In addition to psychomotor retardation, speech delay and seizure disorders, his abnormal phenotypic features included epicanthal folds, broad depressed nasal bridge, protruding thick upper and lower lips, micrognathia, narrow high arched palate, short fifth fingers with a mild degree of clinicodactyly, multiple café-aui-lait spots, and abnormal dermatoglyphics.