The development of comprehension and reading-related skills in children learning English as an additional language and their monolingual, English-speaking peers.

BACKGROUND: A significant number of pupils in UK schools learn English as an additional language (EAL). Relative differences between the educational attainment of this group and monolingual, English-speaking pupils call for an exploration of the literacy needs of EAL learners. AIMS: This study explores the developmental progression of reading and listening comprehension skills and a range of reading-related skills in EAL learners, whose first language is of South Asian origin, and their monolingual peers. SAMPLE: Participants were 39 children learning EAL and 39 monolingual, English-speaking children who were all in school Year 3 at the start of the study. METHOD: Children completed standardized measures of comprehension, vocabulary, reading accuracy, and reading fluency in school Year 3 and again in Year 4. RESULTS: The results suggest that, although children learning EAL often demonstrate fast and accurate reading accuracy skills, lower levels of vocabulary knowledge place significant constraints on EAL learners' comprehension of spoken and written texts. CONCLUSIONS: Reciprocal relationships between vocabulary and comprehension may lead to increasing gaps in reading comprehension between monolingual and EAL pupils over time. It is proposed that support for the development of vocabulary skills in children learning EAL is needed in early years' classrooms.

The comprehension skills of children learning English as an additional language.

BACKGROUND: Data from national test results suggests that children who are learning English as an additional language (EAL) experience relatively lower levels of educational attainment in comparison to their monolingual, English-speaking peers. AIMS: The relative underachievement of children who are learning EAL demands that the literacy needs of this group are identified. To this end, this study aimed to explore the reading- and comprehension-related skills of a group of EAL learners. SAMPLE: Data are reported from 92 Year 3 pupils, of whom 46 children are learning EAL. METHOD: Children completed standardized measures of reading accuracy and comprehension, listening comprehension, and receptive and expressive vocabulary. RESULTS: Results indicate that many EAL learners experience difficulties in understanding written and spoken text. These comprehension difficulties are not related to decoding problems but are related to significantly lower levels of vocabulary knowledge experienced by this group. CONCLUSIONS: Many EAL learners experience significantly lower levels of English vocabulary knowledge which has a significant impact on their ability to understand written and spoken text. Greater emphasis on language development is therefore needed in the school curriculum to attempt to address the limited language skills of children learning EAL.

Dysplastic canine retinal morphogenesis.

Retinal dysplasia is a failure in normal retinal development. The morphologic sequence of the dysplastic processes was examined in fetuses and neonates from dogs affected with an inherited form of retinal dysplasia. The dysplastic change has its onset at 45-50 days' gestation and is most prominent in the dorsal peripapillary retina. Morphologic characteristics of involved sensory retina include the focal loss of cell junctions forming the external limiting membrane, folding of the sensory retina, disorganized proliferation of neuroblasts in the retina and subretinal space, and formation of rosettes composed of multiple layers of neuroblasts. These morphologic changes suggest that there is an intrinsic abnormality of neural retinal differentiation.

Ocular infection with a murine neurovirulent retrovirus does not cause retinal degeneration.

The developing eyes of CFW/D mice inoculated at birth with a neurovirulent mutant (ts1) of Moloney murine leukemia virus (MoMuLV), nonneurovirulent wild type (wt) MoMuLV, and conditioned virus-free medium were studied comparatively by immunohistochemistry, lectin histochemistry and light microscopy. Cellular targets for viral antigen expression in the eye were identical in both ts1 and wt MoMuLV-infected mice. Viral antigen first was observed in endothelial cells of the retina and subsequently spread in a spatial and temporal pattern consistent with normal vascularization of the developing retina. The virus also was observed in (1) epithelial cells of the bulbar and palpebral conjunctiva, ora ciliaris retinae, and lacrimal gland; (2) endothelial cells of the ciliary body, iris, choroid, and sclera; (3) amacrine cells of the retina; and (4) smooth muscle cells and endothelia of the periocular muscle. Although ts1 MoMuLV induced a spongiform encephalopathy in the brain and spinal cord, structural lesions were not observed in the retina or other ts1 MoMuLV-infected ocular structures; differentiation of the retina was normal. The lectin Ricinus communis agglutinin-I (RCA-I) labeled (1) endothelial cells of the hyaloid vessels, tunica vasculosa lentis, retina, ciliary body, iris, choroid, and sclera; (2) epithelial cells of the cornea, bulbar and palpebral conjunctiva, ora ciliaris retinae, and lacrimal gland; (3) smooth muscle cells and endothelia of the periocular muscle; (4) inner segments of the photoreceptor layer; and (5) amacrine cells of the retina.(ABSTRACT TRUNCATED AT 250 WORDS)

Glomerulopathy in squirrel monkeys with acute Plasmodium falciparum infection.

The renal pathology of 9 squirrel monkeys (Saimiri sciureus) with acute Plasmodium falciparum infection was studied by light and electron microscopy. Endocapillary proliferative glomerulonephritis was the major pathological change observed. The peroxidase anti-peroxidase method demonstrated the presence of IgG, IgM, and P. falciparum antigens in the mesangium and basement membrane. These findings were consistent with those seen in humans with acute P. falciparum infection and indicates that squirrel monkeys are likely to be a good model for the study of renal pathology in malaria research.

Pathologic changes associated with fatal Plasmodium falciparum infection in the Bolivian squirrel monkey (Saimiri sciureus boliviensis).

Fatal cases of experimental Plasmodium falciparum (Indochina I) in Bolivian squirrel monkeys (Saimiri sciureus boliviensis) were examined by histologic and ultrastructural methods. Gross lesions were characterized by hepatosplenomegaly and interstitial pulmonary changes. Histologically, there was marked diffuse reticuloendothelial hyperplasia, pulmonary alveolar septal thickening, mesangioproliferative glomerulonephropathy, sequestration of parasitized erythrocytes in deep vascular beds, degenerative parenchymal changes in the liver and myocardium, and in one case retinal and cerebral hemorrhage. These data indicate that the Bolivian squirrel monkey is a good model for studying pathologic changes associated with human falciparum malaria.

Peroxisome proliferator-activated receptor alpha-null mice lack resistance to acetaminophen hepatotoxicity following clofibrate exposure.

The purpose of this study was to investigate whether activation of the nuclear receptor PPARalpha is needed for protection from acetaminophen (APAP) hepatotoxicity produced by repeated administration of the peroxisome proliferator clofibrate (CFB). Female wild-type and PPARalpha-null mice received corn oil vehicle or 500 mg CFB/kg, ip, daily for 10 days. They were then fasted overnight (18 h) and either killed at 4 or 24 h after challenge with 400 mg APAP/kg. Controls received 50% propylene glycol vehicle only. In this model of CFB hepatoprotection, liver injury was assessed by measuring plasma sorbitol dehydrogenase activity and by histopathology at 24 h after APAP challenge. Significant hepatocellular necrosis was evident in both corn oil-pretreated PPARalpha-null and wild-type mice at 24 h after APAP challenge. In agreement with previous studies, CFB-pretreated wild-type mice showed marked protection against APAP toxicity. In contrast, CFB did not provide protection against APAP hepatotoxicity in the PPARalpha-null mice. Similarly, at 4 h after APAP challenge, hepatic glutathione depletion and selective arylation of cytosolic proteins were reduced significantly in CFB-pretreated wild-type mice, but not in PPARalpha-null mice. The lack of changes in APAP binding and NPSH depletion in CFB-pretreated, PPARalpha-null mice is consistent with the presence of significant liver injury at 24 h in this treatment group. These findings demonstrate that the protection against APAP hepatotoxicity by peroxisome proliferator treatment is mediated by the activation of PPARalpha.

Repeated dosing with the peroxisome proliferator clofibrate decreases the toxicity of model hepatotoxic agents in male mice.

Pretreatment of mice with clofibrate (CFB) has been shown to protect against acetaminophen (APAP) hepatotoxicity. To determine if pretreatment with CFB prevents the toxicity of other model hepatotoxicants, male C57BL6J or CD-1 mice received 500 mg CFB/kg, i.p., daily for 10 days, and then were challenged with either 250 mg bromobenzene (BrB)/kg, 0.025 ml carbon tetrachloride (CCl4)/kg or 0.5 ml chloroform (CHCl3)/kg. Liver and kidney injury was assessed by plasma sorbitol dehydrogenase activity (SDH) and blood urea nitrogen (BUN), respectively and histopathology. Challenge with BrB significantly elevated plasma SDH activity in C57Bl6J mice. This was prevented in CFB pretreated mice receiving the same dose of BrB. Changes in BUN were not detected in either group of BrB treated mice. Similarly, pretreatment of male CD-1 mice with CFB significantly reduced CCl4-induced elevation in plasma SDH activity, with no BUN elevation detected in either group. CFB pretreatment also diminished elevation in plasma SDH activity produced by CHCl3 in CD-1 mice, while BUN was significantly elevated in both groups, indicating that CFB did not protect against CHCl3-induced nephrotoxicity. Histopathological examination of liver and kidney sections confirmed these results. This study shows that mice pretreated with CFB were protected from toxicity at 24 h after challenge with other model hepatotoxic agents besides APAP.

Changes in susceptibility to acetaminophen-induced liver injury by the organic anion indocyanine green.

The non-metabolizable organic anion indocyanine green (ICG) has been shown previously to reduce markedly the biliary secretion of acetaminophen, particularly the glutathione conjugate of APAP (APAP-GSH), suggesting that this APAP metabolite may compete with other xenobiotics for excretion into the bile via a canalicular organic anion transport process. This study was conducted to determine whether changes in the biliary disposition of APAP induced by ICG could lead to alterations in susceptibility to APAP hepatotoxicity. To investigate this, groups of overnight-fasted male CD-1 mice received 30 micromol ICG/kg, intravenously, immediately prior to APAP dosing (500 mg/kg, ip). Controls were given propylene glycol vehicle. Mice were killed at 4 h after APAP challenge for immunochemical analysis of cytosolic protein arylation and determination of non-protein sulfhydryl (NPSH) depletion, or at 12 and 24 h for biochemical and histological assessment of liver injury. Elevated plasma sorbitol dehydrogenase activity and centrilobular hepatocellular necrosis was present in control mice receiving APAP at 12 and 24 h. Treatment with ICG did not alter susceptibility to APAP toxicity when measured at 12 h after challenge. However, the severity of histologic lesions in the ICG-APAP group was significantly lower at 24 h after challenge. Furthermore, treatment with ICG did not alter APAP-induced glutathione depletion or cytosolic protein arylation. These data suggest that the organic anion ICG has a protective effect on APAP toxicity that promotes a faster recovery from liver injury.

The PPAR activator docosahexaenoic acid prevents acetaminophen hepatotoxicity in male CD-1 mice.

Acetaminophen (APAP)-induced hepatocellular necrosis can be prevented by treatment with peroxisome proliferators. This protection is associated with lowered protein arylation and glutathione depletion in mice. Peroxisome proliferators have been shown to activate nuclear receptors. These receptors, termed peroxisome proliferator activated receptors (PPARs), can also be activated by free fatty acids. This study was designed to determine if treatment with the PPAR activator docosahexaenoic acid (DHA) would also lower APAP toxicity. Male CD-1 mice received 250 mg DHA/kg or 500 mg clofibrate (CFB)/kg, i.p., for 5 d. Controls received corn oil vehicle, i.p. After overnight fasting, mice received 800 mg APAP/kg, p.o. At 24 h after APAP, hepatotoxicity was evident in control mice by elevated plasma sorbitol dehydrogenase activity (SDH) and histologic evidence of hepatic degeneration and necrosis. As expected, CFB pretreatment significantly decreased this. Similarly, DHA protected against APAP-induced hepatotoxicity at 24 h after challenge. However, treatment with DHA did not increase hepatic glutathione prior to APAP, as previously shown with CFB. Interestingly, DHA did not increase palmitoyl coenzyme A (CoA) oxidase activity or other biochemical parameters associated with peroxisome proliferation after 5 d of treatment at 250 mg/kg. No significant alterations in microsomal APAP glucuronidation or cytochrome P-450-mediated bioactivation were detected either. Collectively, these results show that DHA also prevents APAP-induced hepatotoxicity at 24 h after challenge. However, the association between resistance against APAP-induced liver injury, PPAR activation, and peroxisome proliferation is not clearly understood.

Intramembranous particle distribution and filipin binding in dysplastic canine retina.

We examined dysplastic canine retina for changes in intramembranous particle (IMP) density and filipin binding to sterols. Differences in IMP density were identified in incipiently dysplastic fetal retina and also in the degree of filipin binding near the onset of the dysplastic process. The data suggest that there are temporal differences in IMPs and filipin-sterol complexes that may be related to the formation of retinal folds and disorganized dysplastic retina proliferation.

The external limiting membrane in developing normal and dysplastic canine retina.

Development of the external limiting membrane of the retina in English springer spaniel fetuses and neonates with incipient stages of retinal dysplasia and in normal mongrel fetuses and neonates was examined using transmission electron microscopy and the freeze-fracture technique. The external limiting membrane of the retina of normal canine fetuses was composed of zonulae adherentes in which there were focal areas of apparent apposition between adjacent ventricular cell membranes. Freeze-fracture examination revealed gap junctions within the external limiting membrane that were composed of 8-10 nm P-face particles in aggregates of variable size and shape. These junctions corresponded to areas of focal membrane apposition. Tight junction strands were also identified in deep E-face grooves which were located perpendicular to the external limiting membrane. At day 46 of gestation in incipiently dysplastic English springer spaniel fetal eyes, there was a marked decrease in the size and area occupied by gap junctions within the external limiting membrane as compared with retinas of mongrel control fetuses at the same age and of other age groups. This apparent loss of gap junctions, coincident with the incipient onset of histologically detectable dysplastic events in the sensory retina, may contribute to the morphogenesis of the defect.

Cilia in the fetal and neonatal canine retina.

Cilia in the canine retina were examined at 40, 46 and 50 days of gestation and at birth by scanning electron microscopy, transmission electron microscopy, and by the freeze-fracture technique. Cilia were similar in all age groups examined. Scanning electron micrographs showed them to be smooth-surfaced conical to tubular extensions arising from putative photoreceptor inner segments. Cilia when freeze-fractured contained variable numbers of circumferential rows of 10 nm P-face particles: these constitute the ciliary necklace. Transmission electron micrographs showed the ciliary membrane to contain electron-dense beads which corresponded to the ciliary necklace seen in freeze-fracture replicas. The ciliary necklace identified in the developing canine retina was similar to those found in other types of motile and sensory cilia.

Identification of Ehrlichia risticii as the causative agent of two equine abortions following natural maternal infection.

Two pregnant mares diagnosed as having equine monocytic ehrlichiosis based on history, clinical signs, and high serum antibody titers to Ehrlichia risticii aborted subsequent to recovery from illness. Mare 1 and mare 2 experienced clinical illness at 120 and 143 days of gestation and aborted at 203 and 226 days of gestation, respectively. The fetuses were expelled in fresh condition, and both mares retained their placentas upon abortion. Gross findings for the fetuses included meconium staining and petechiation of external surfaces. Internally, there was increased volume of feces within the small and large intestines and liver discoloration with enlargement. Microscopic findings included lymphohistiocytic enterocolitis, hepatitis, and myocarditis. Lymphoid hyperplasia and depletion were present in spleen, thymus, and lymph nodes. Ehrlichia risticii was recovered from bone marrow, spleen, lymph node, colon, and liver of the first fetus and bone marrow and colon of the second fetus. Electron microscopic evaluation of the organism isolated in cell culture revealed morphology consistent with E. risticii. The isolated organism was inoculated into a naive pony, and this pony developed high levels of antibody against E. risticii, became ehrlichemic, and developed clinical signs of depression, anorexia, and mild diarrhea. These findings confirm that E. risticii is an abortifacient under conditions of natural infection and should be considered as a differential diagnosis of equine abortions.

Papillomavirus infection of aged Persian cats.

Papillomavirus infection was confirmed in 2 Persian cats with sessile hyperkeratotic skin lesions. Skin lesions were not typical papillomas as found in other species. Papillomavirus were demonstrated in negative stain preparations of homogenized tissue and within nuclei of cells in the stratum granulosum. Papillomavirus group-specific antigens were detected within nuclei corresponding to those containing virions. Attempts to transmit this disease to other cats or propagate the virus in tissue cultures were unsuccessful. A 7.8-kilobase DNA molecule was present in low-stringency Southern blots using a bovine papillomavirus type 1 cloned DNA probe. In reverse Southern blots, the cat papillomavirus hybridized under conditions of low stringency with all papillomavirus genomes tested. Combined with limited restriction endonuclease restriction mapping, the above information indicates that the feline cutaneous papillomavirus is a unique virus type and thus expands the list of hosts known to be infected by papillomaviruses.

Expression of lectin binding in cutaneous papillomas of animals.

A group of spontaneously occurring animal papillomas which were negative or positive for papillomavirus group-specific antigen were examined with a battery of biotinylated lectins including Con A, WGA, succinylated-WGA, PNA and UEA-I. Canine papillomas, equine papillomas, white-tailed deer fibromas, mule deer fibromas, and bovine fibropapillomas were examined. Each lectin had a specific staining pattern. No obvious differences in staining patterns between normal skin, viral antigen-positive and -negative neoplasms were identified. This may be due to the well-differentiated and organized nature of these tumours.

Argyrophilic, intracellular bacteria in some cats with idiopathic peripheral lymphadenopathy.

Lymph node biopsy specimens from several previously reported cases of unusual feline peripheral lymphadenopathies were re-examined by a modified Dieterlé silver-impregnation staining technique. In a proportion of these specimens, the Dieterlé stain revealed tiny pleomorphic, intensely argyrophilic coccobacilli. These organisms were predominantly located within macrophages. The infected cells were focally distributed, particularly in the interfollicular regions of the nodes. They were inconspicuous in sections stained by other, more conventional staining methods. It is possible that these coccobacilli represent yet another, previously unidentified, cause of chronic lymph node hyperplasia in the cat.

Black walnut (Juglans nigra) toxicosis: a model for equine laminitis.

Twelve light horse geldings developed laminitis within 8 to 12 h of being dosed by nasogastric tube with an aqueous extract of black walnut (Juglans nigra). Four of the 12 horses developed the severe signs of grade 3 laminitis (lame at a walk, refused to lift feet). Laminitis was accompanied by mild depression and limb oedema. There was no evidence of shock or colic. The horses developed neutropenia by 4 h after dosing with the extract, which shifted to a relative neutrophilia by 8 to 12 h. Minimal increases in plasma epinephrine and cortisol concentrations were suggested in severely affected horses. Severe laminitis was characterized by necrosis of dermal tips of dorsal primary epidermal laminae. A proliferative epithelial response in these laminae was distinguished by numerous mitotic figures and clusters of epithelial cells. This evidence suggests that black walnut toxicosis is not only a consistent clinical model, but is also a reliable clinico-pathological and pathological model for study of the pathogenesis and treatment of laminitis.

Effects of inflammation and aqueous tear film deficiency on conjunctival morphology and ocular mucus composition in cats.

An experimental model of keratoconjunctivitis sicca (KCS) was produced by removing the lacrimal gland and the gland of the third eyelid from the left eye of 6 cats. The right eye of each cat was left intact and used as a control. After 2 weeks, cats were euthanatized and the central portion of the upper eyelid from both eyes of each cat was excised. Histologic sections were stained with either hematoxylin and eosin or with a battery of biotinylated lectins including concanavalin A (conA), soybean agglutinin (SBA), wheat germ agglutinin (WGA), succinylated wheat germ agglutinin (S-WGA), Ulex europaeus agglutinin I (UEA), Dolichos biflorus agglutinin (DBA), Ricinus communis agglutinin (RCA), peanut agglutinin (PNA), and PNA pretreated with neuraminidase. Consistent differences in histologic features were not observed between conjunctivas with KCS and control conjunctivas. A variable degree of mononuclear cell infiltration of the substantia propria was observed in control conjunctivas and those with KCS. In both groups, conjunctival goblet cell density decreased and epithelial stratification increased as the degree of submucosal inflammatory cell infiltration increased. Lectin binding sites for DBA, WGA, S-WGA, UEA, PNA, and PNA pretreated with neuraminidase were detected on conjunctival goblet cells of conjunctivas with KCS and control conjunctivas. The mucus/glycocalyx layer of conjunctival epithelial cells in both groups of conjunctivas bound lectins RCA, WGA, UEA, and conA, but inconsistently bound S-WGA. In both groups, DBA principally bound to the mucus layer overlying normal epithelium, whereas PNA pretreated with neuraminidase consistently bound to the mucus layer of stratified epithelial surfaces free of goblet cells. Binding of SBA to goblet cells and the mucus/glycocalyx layer was variable.

Evaluation of fetal infection and abortion in pregnant ponies experimentally infected with Ehrlichia risticii.

Fetal infectivity of Ehrlichia risticii was investigated in 19 ponies that were E risticii negative on the basis of results of an indirect fluorescent antibody (IFA) test. Thirteen pregnant ponies were infected by IV administration of E risticii between 90 and 180 days of gestation. Six pregnant ponies served as noninfected controls. Each infected pony had clinical signs of equine monocytic ehrlichiosis, was confirmed to be ehrlichemic, and developed an IFA titer to E risticii. Two infected ponies became recumbent, were unresponsive to supportive care, and were euthanatized. After recovery from clinical illness, the remaining ponies were observed throughout gestation for reproductive abnormalities. On abortion, each fetus was necropsied and tissue specimens from the liver, bone marrow, spleen, colon, and mesenteric lymph nodes were inoculated into canine monocyte cell cultures. Six infected ponies aborted at a mean 217 days of gestation, which was between postinoculation days 65 and 111. Five fetuses were recovered for evaluation, and E risticii was isolated from 4 of them. All 5 fetuses recovered had similar histologic finding, including enterocolitis, periportal hepatitis, and lymphoid hyperplasia with necrosis of the mesenteric lymph nodes and spleen. All 5 fetuses tested negative for IgG to E risticii, although 3 had low IgM titer to E risticii. The remaining 5 infected ponies had normal parturition. Presuckle IFA titer to E risticii was measured in 4 of the term foals, and results for 3 were positive. Two foals from infected ponies were monitored for 6 months and daily gain in body weight was comparable to that of a control foal. None of the control ponies became ill or seroconverted during the clinical illness phase, and none aborted throughout gestation Two control ponies seroconverted to E risticii 6 weeks before parturition. Results of this study indicate that E ristcii is a primary abortifacient under experimental conditions.