Postnatal white matter necrosis in preterm infants.

One hundred twenty-seven infants less than 36 weeks of gestation (mean +/- SE = 31 +/- 3.2 weeks) were studied with echoencephalography to determine the incidence and complications associated with white matter necrosis. Ten infants (8%) developed cysts ten or more days after birth, indicating postnatal onset of white matter necrosis. Univariate analysis showed that postnatal white matter necrosis was significantly associated with maternal infection (other than urinary infection), respiratory distress syndrome, and longer requirement of an oxygen concentration greater than 40%. Forward logistic regression analysis showed postnatal white matter necrosis to be associated with maternal infection, chronic placental infarction, congenital pneumonia, and longer requirement of an oxygen concentration greater than 40%. Neurodevelopmental outcome was abnormal during infancy in 4 of the 6 survivors with postnatal white matter necrosis. Severe respiratory disease and maternal and/or fetal infection appear to increase the risk of the immature brain to white matter necrosis, predisposing the infants to subsequent neurodevelopmental delay.     

RT-PCR-RFLP for genetic diversity analysis of Tunisian Grapevine fanleaf virus isolates in their natural host plants

Genetic diversity was characterized in 20 isolates of Grapevine fanleaf virus (GFLV) recovered from naturally infected grapevine plants (Vitis vinifera) in the North of Tunisia. Viral RNAs were isolated by oligoprobe capture, and a 605 bp fragment containing a part of the viral coat protein gene was amplified by RT-PCR. Sequence variation among isolates was characterized by restriction fragment length polymorphism (RFLP) analysis and confirmed by sequencing. The GFLV infections are found as a complex mixture of closely related genomes. In further studies, RFLP analyses of virus isolates using AluI showed that GFLV populations in Tunisian vineyards consist of two restrictotypes corresponding to distinct sub-populations Sp1 and Sp2. The relative field distribution of these sub-populations showed that Sp2 was more abundant. Individual genomes were recovered by cloning the RT-PCR products. The sequences were found to vary from each other by as much as 11%. Cloning from mixed infections showed that Sp2 are also predominant.     

Pyogenic granuloma-like reaction in the necrotic, vessels-deprived femoral head of the rat

Osteonecrosis of the femoral head was produced in rats by cutting the ligamentum teres and incising the cervical periosteum. As of the second postoperative week, fibrous tissue pervaded the necrotic epiphyses, macrophages and osteoclasts removed the debris, osteoblasts deposited lamellar-fibred and woven-fibred intramembranous bone, and remodeling began. In 16% of the rats killed during the 2nd postoperative week, the epiphyses contained big fragments of necrotic bone enclosed by densely packed, capillary-sized vessels. Ingrowth of this hypervascularized, pyogenic granuloma-like tissue is presumably due to the presence of excessive growth factors, reflecting an exaggerated pathophysiological reaction within the framework of organization of the necrotic epiphyses.     

Effect of rivastigmine on scopolamine-induced memory impairment in rats

The effect of rivastigmine on memory impairments induced in rats by scopolamine (0.5 mg/kg) was assessed in the Morris water maze and passive avoidance tests and compared with that of tacrine (2.5-17.7 mg/kg). Rivastigmine, (0.5-2.5 mg/kg) inhibited cholinesterase in the cortex and hippocampus by 21-60% and antagonised the deficits in working and reference memory. Tacrine (12.5 and 17.7 mg/kg) produced significantly less inhibition of cholinesterase in the hippocampus but more in the striatum than rivastigmine (0.75 and 1.5 mg/kg) and only antagonised the deficit in reference memory. Rivastigmine (1.5 and 2.5 mg/kg) or tacrine (12.5 mg/kg), injected immediately after completion of the acquisition trial in the passive avoidance test, antagonised the deficit induced by scopolamine (1 mg/kg) in memory retention. The inability of higher doses of the cholinesterase inhibitors to antagonise memory deficits induced by scopolamine may be related to excessive cholinergic stimulation in the central nervous system.     

The expression of lysyl‐oxidase gene family members in myeloproliferative neoplasms

Myeloproliferative neoplasms (MPNs) are malignant disorders originating from clonal expansion of a single neoplastic stem cell and characteristically show an increase in bone marrow reticulin fibers. Lysyl oxidases (LOXs) are copper‐dependent amine oxidases that play a critical role in the biogenesis of connective tissue by crosslinking extracellular matrix proteins, collagen and elastin. Expression of LOX gene family members is increased in disorders associated with increased fibrosis. To evaluate involvement of LOX gene family in various MPNs. In‐situ hybridization was used to detect Lysyl‐Oxidase family members in bone marrow biopsies from patients with different MPNs. We compared normal bone marrows and those from patients with polycythemia vera, essential thrombocythemia, chronic myeloid leukemia, and primary myelofibrosis (PMF). Serum levels of lysyl‐oxidase from patients with PMF and healthy controls were also examined. LOX gene family was not detected in normal bone marrows. All members of the LOX gene family were over expressed in PMF. In other MPNs a differential pattern of expression was observed. Differences in gene expression were statistically significant (P < 0.010). The medianserum LOX levels in normal controls was 28.4 ± 2.5 ng\ml and 44.6 ± 9.44 ng\ml in PMF (P = 0.02). The varying pattern of expression of LOX genes may reflect differences in the pathophysiology of bone marrow fibrosis in these MPNs. These observations could be used as the basis for future targeted therapy directed against bone marrow fibrosis. Am. J. Hematol. 88:355–358, 2013. © 2013 Wiley Periodicals, Inc.     

Topical interferon alpha 2 beta therapy in the management of conjunctival papilloma.

BACKGROUND: This article describes the differential diagnosis of conjunctival papillomas and reviews the treatment options with a focus on the new topical interferon alpha 2 beta therapy. CASE: A 45-year-old white man presented with a red right eye of approximately 6 months' duration. The lesion was suspicious and suggestive of malignancy; therefore, the patient was referred for consultation. The lesion was diagnosed as a conjunctival papilloma. The patient was placed on topical interferon alpha 2 beta eye drops, and within 2 weeks he experienced complete lesion regression. CONCLUSION: Interferons, in particular interferon alpha-2b (IFN-alpha2beta), have recently been shown to be successful in treating conjunctival papillomas and conjunctival intraepithelial neoplasia (CIN). Previously, treatment was limited to observation for asymptomatic patients. Larger lesions in symptomatic patients were treated by surgical excision and cryotherapy. Additional treatment modalities included topical antimetabolite treatment with mitomycin-C and 5-fluorouracil. These treatments, although effective, had significant attendant postsurgical complications and toxic ocular adverse reactions. Interferons represent a new successful treatment modality.     

Intracerebroventricular injection of streptozotocin causes neurotoxicity to myelin that contributes to spatial memory deficits in rats

It has been reported that intracerebroventricular (icv) injection of streptozotocin (STZ) impairs spatial memory by disrupting glucose utilization through an insulin-dependent mechanism in the cerebral cortex and hippocampus. However, evidence of septal damage and microglosis induced by icv STZ suggested that its neurotoxic effects could contribute to the memory impairment. The present study examined the histopathological changes in adult rats following three icv STZ injections (0.25 mg into each lateral ventricle) and their effects on spatial memory in a Morris water maze task. STZ retarded acquisition of reference learning (progressive reduction in escape latency) and disrupted working memory (difference in escape latency between the two swims within a daily session). STZ caused selective injury to myelin and axons in the fornix and hippocampus in association with activation of microglia. The 3rd ventricle was enlarged by 100-150% because of a loss of ependymal cells and damage to hypothalamic periventricular myelin but the process involved in these changes is unclear. Our findings provide an alternative explanation for the decrease in glucose utilization in the hippocampus and cortex and the impairment of spatial memory induced by STZ. These could result from a disruption of the communication through myelinated axons in the fornix connecting the septum and the hippocampus, and through other myelinated axons adjacent to the ventricles. The selective damage to myelin may well result from oxidative stress.