Larval nutritional-stress and tolerance to extreme temperatures in the peach fruit fly, Bactrocera zonata (Diptera: Tephritidae).

Within the factors affecting insect tolerance to extreme environmental conditions, insect nutrition, particularly of immature stages, has received insufficient attention. In the present study, we address this gap by investigating the effects of larval nutrition on heat and cold tolerance of adult Bactrocera zonata - an invasive, polyphagous fruit fly pest. We manipulated the nutritional content in the larval diet by varying the amount of added yeast (2-10% by weight), while maintaining a constant sucrose content. Adults derived from the different larval diets were tested for their tolerance to extreme heat and cold stress. Restricting the amount of yeast reduced the efficacy of the larval diet (i.e. number of pupae produced per g of diet) as well as pupal and adult fresh weight, both being significantly lower for yeast-poor diets. Additionally, yeast restriction during the larval stage (2% yeast diet) significantly reduced the amount of protein but not lipid reserves of newly emerged males and females. Adults maintained after emergence on granulated sugar and water for 10 days were significantly more tolerant to extreme heat (i.e. knock-down time at 42 oC) when reared as larvae on yeast-rich diets (8% and 10% yeast) compared to counterparts developing on a diet containing 2% yeast. Nevertheless, the composition of the larval diet did not significantly affect adult survival following acute cold stress (exposure to -3°C for 2 hrs.). These results are corroborated by previous findings on Drosophilid flies. Possible mechanisms leading to nutrition-based heat-tolerance in flies are discussed.

Tumor necrosis factor alpha and lymphotoxin alpha are not required for induction of acute experimental autoimmune encephalomyelitis.

Immunization of mice with myelin components results in experimental autoimmune encephalomyelitis (EAE), which is mediated by myelin-specific CD4(+) T cells and anti-myelin antibodies. Tumor necrosis factor alpha (TNF-alpha) and lymphotoxin alpha (LT-alpha) are thought to be involved in the events leading to inflammatory demyelination in the central nervous system. To ascertain this hypothesis 129 x C57BL/6 mice with an inactivation of the tnf and lta genes (129 x C57BL/6(-/-)) and SJL/J mice derived from backcrosses of the above mentioned mutant mice (SJL-/-) were immunized with mouse spinal cord homogenate (MSCH) or proteolipid protein. Both 129 x C57BL/6(-/-) mice and SJL-/- mice developed EAE. In SJL-/- mice immunized with MSCH, a very severe form of EAE with weight loss, paralysis of all four limbs, and lethal outcome was observed. The histologic hallmark was an intense perivascular and parenchymal infiltration with predominantly CD4(+) T cells and some CD8(+) T cells associated with demyelination in both brain and spinal cord. These results indicate that TNF-alpha and LT-alpha are not essential for the development of EAE.

Endoscopic management of a rare case of nasal glioma in Meckel's cave in an adult: case report.

BACKGROUND: Nasal glioma or glial heterotopia is a rare embryologic anomaly that heralds its presence shortly after birth or in childhood. Nasal glioma in an adult is very rare, often asymptomatic and the occurrence of nasal glioma in Meckel's cave in an adult has not been previously reported. CASE REPORT: The authors encountered a case of an incidentally diagnosed Meckel's cave nasal glioma in a 40-year-old male which was successfully excised by an endonasal endoscopic transmaxillary transpterygoid approach. CONCLUSION: The occurrence of a nasal glioma in Meckel's cave an adult is very rare. Considering the deep skull base location, endonasal endoscopic surgery provides a minimal access technique to reach this location with excellent results.

Coronavirus infection induces H-2 antigen expression on oligodendrocytes and astrocytes.

Infection of the central nervous system by mouse hepatitis virus strain A59, a murine neurotropic coronavirus, induces class I major histocompatibility complex antigens on mouse oligodendrocytes and astrocytes, cells that do not normally express these antigens on their surfaces. This induction, which occurs through soluble factors elaborated by infected glial cells, potentially allows immunocytes to interact with the glial cells and may play a critical role in the pathogenesis of virus-induced, immune-mediated demyelination in the central nervous system.

Infection of the basal ganglia by a murine coronavirus.

The coronavirus, mouse hepatitis virus strain A59 (MHV-A59), causes mild encephalitis and chronic demyelination. Immunohistochemical techniques showed that MHV-A59-infected C57BL/6 mice contained dense deposits of viral antigen in the subthalamic nucleus and substantia nigra, with fewer signs of infection in other regions of the brain. The animals showed extra- and intracellular vacuolation, neuronal loss, and gliosis in the subthalamic-nigral region. Such localization is unprecedented among known viral encephalitides of humans and other species. This infection by a member of a viral class capable of causing both encephalitis and persistent infection in several species may be related to postencephalitic parkinsonism.

Endovascular treatment of isolated dissecting aneurysm of the posterior inferior cerebellar artery.

BACKGROUND AND PURPOSE: Isolated dissecting aneurysms of the posterior inferior cerebellar artery (PICA) carry a high risk of rebleeding with an associated increased mortality rate. Although rare, they present a therapeutic challenge. Surgical treatment carries a significant risk of neurologic complications, predominantly lower cranial nerve deficits because of the close relationship of the aneurysm with the brain stem and cranial nerves. The purpose of this article is to show that endovascular treatment of dissecting aneurysms of the PICA can be effective and can allow the patient to avoid the complications associated with surgery. METHODS: Six patients (age range, 28-70 years) with dissecting aneurysms of the PICA were treated at our center by endovascular occlusion with Guglielmi detachable coils or glue and followed for up to 30 months. Inclusion of patients in the study was based on careful angiographic assessment of the vascular anatomy and collateral supply of the posterior fossa. When on the basis of the anatomy, potential lack of sufficient collaterals was suggested, a test occlusion was performed to determine the feasibility of an endovascular approach. Four additional cases, which have been described in the literature, were included in the analysis of results. RESULTS: In all patients, the aneurysm was successfully occluded with no apparent procedure-related complications. Follow-up studies showed stable and complete occlusion of the aneurysm in all patients with no long-term neurologic deficits. CONCLUSIONS: Endovascular treatment by aneurysm and parent artery occlusion is a relatively safe and reliable alternative to surgery for isolated dissecting aneurysms of the PICA.

Cellular reservoirs of HIV-1 in the central nervous system of infected individuals: identification by the combination of in situ polymerase chain reaction and immunohistochemistry.

OBJECTIVES: The majority of HIV-1-infected individuals manifest a plethora of central nervous system (CNS) diseases unrelated to opportunistic infections, including AIDS dementia complex, encephalitis, and various other disorders of the CNS. The present study sought to evaluate the cellular reservoirs and expression patterns of HIV-1 in brain tissue to gain further understanding of HIV-1 neuropathogenesis. DESIGN: CNS tissue, obtained post-mortem from 22 patients with AIDS and four HIV-1-seronegative controls, was analyzed. METHODS: CNS samples were evaluated using a combination of in situ DNA polymerase chain reaction (PCR), reverse transcriptase (RT)-initiated in situ PCR, and immunohistochemistry. By utilizing this triple-staining methodology, HIV-1 proviral DNA and HIV-1-specific mRNA can be identified at the single cell level. RESULTS: HIV-1 was detected in all 22 AIDS brain specimens and in none of the four brains from HIV-1-seronegative individuals. The most commonly infected cells in AIDS brains were microglia cells and macrophages, but variable levels of HIV-1 infections were demonstrated in many of the major histological cell types within the CNS, including neurons, microvascular endothelial cells (MVEC) and astrocytes. The presence of HIV-1-infected cells was not uniform with infected cells unevenly distributed throughout the brain parenchyma. The degree of HIV-1 mRNA expression varied from 39-65% of the cells in the CNS harboring HIV-1 provirus. Choroid plexus and MVEC exhibited relatively high levels of productive infection. CONCLUSION: These findings demonstrate that several cell types in the CNS, in addition to microglia or macrophages, may become infected with HIV-1 in vivo with variable levels of HIV-1 mRNA expression. The diverse cellular reservoirs for HIV-1 in the CNS may be critically linked to the molecular mechanisms involved in HIV-1 neuropathogenesis. In addition, in vivo infection of MVEC, and possibly cells in the choroid plexus, may directly contribute to penetration of the blood-brain barrier by HIV-1.

Nidovirus infections: experimental model systems of human neurologic diseases.

The presence of terminally differentiated slow- and non-dividing cells in the central nervous system (CNS) provides a safe harbor for viral persistence and latency and constitutes a unique immunologic environment for viral infections. Studies of experimental model systems of viral infections of the CNS provide insight into mechanisms of viral persistence and immune-mediated pathology. Nidoviruses are comprised of 2 families of viruses, coronaviruses and arteriviruses, and are common pathogens of humans and a variety of animal species. Both families of viruses contain neurotropic strains that produce experimental neurologic diseases in rodents. These include acute meningitis and encephalitis; acute poliomyelitis; and chronic inflammatory, immune-mediated, demyelination. Coronavirus-induced demyelinating disease mimics many of the pathologic features of Multiple Sclerosis (MS).

Expression pattern of CXCR3, CXCR4, and CCR3 chemokine receptors in the developing human brain.

Chemokine receptors are essential components of the immune and central nervous systems, but little is known about their distribution during development. We evaluated the distribution of 3 chemokine receptors: CXCR3, CXCR4, and CCR3 in the human developing brain. Of these, CXCR3 was the only receptor expressed in fetal brain at 26 wk of gestation and its expression was restricted to glial cells, endothelial cells, and the choroid plexus. Neuronal staining was only seen at term in the Purkinje cells of the cerebellum. CCR3 appeared only at term in both neurons and glial cells. The expression pattern of these 2 receptors in the late gestation and term resembled that of adults. CXCR4 could not be detected in the fetal brain on neurons nor on glial cells. By examining pediatric cases, we determined that CXCR4 expression commences sometimes between 3.5 and 4.5 yr. Two of the chemokine receptors examined, CCR3 and CXCR4, can be used as co-receptor together with CD4 for HIV entry, but neither was expressed during the second trimester of pregnancy. Our findings suggest that it is unlikely that CCR3 or CXCR4 play a major role in HIV-1 transmission in the fetal brain before 37 wk of gestation.

Case of the month: April 1997--a 32 year old man with mental status changes and a severe occipital headache.

A 32 year old man with symptoms of an upper respiratory infection one week prior presented with mental status changes, diffuse hyperreflexia, and bilateral extensor plantar responses. An MRI scan showed multifocal areas of high signal intensity predominantly in the parietal and occipital white matter, unassociated with mass affect. Despite aggressive treatment, the patient's symptoms rapidly progressed and he was declared brain dead. Post-mortem examination revealed acute hemorrhagic leukoencephalopathy. The clinical and pathologic features of this disorder are reviewed.

Case of the month: March 1998--48 year old man with back pain and weakness.

A 48 year old man with long history of end stage renal disease (ESRD) and secondary hyperparathyroidism presented with back pain and incontinence. MRI and CT showed T2 expansion with bony destruction and spinal cord compression. Other vertebral bodies showed destructive lesions as well. Microscopic examination showed a brown tumor composed of multinucleated giant cells and bone uninvolved by tumor showed "tunneling" resorption. Brown tumors are an exaggerated form of "local" osteitis fibrosa cystica in patients with ESRD and secondary hyperparathyroidism, but spinal cord compression is rare.

Case of the month: May 1998--a patient with HIV infection and multiple cranial neuritis.

A 36-year old male with a three year history of HIV infection and more recently, CMV retinitis, had several episodes of polyradiculitis with severe bilateral leg pain and urinary retention which resolved slowly over several months. He then presented with high fevers and severe dysphagia with dehydration. Examination showed oral thrush, dyarthric speech and mild memory impairment. Fundoscopic exam showed CMV retinitis and HIV retinopathy. Further examination revealed other cranial nerve signs and leg weakness. MRI scans showed several contrast enhancing abnormalities of cranial nerve roots. The patient died from massive barium aspiration. At autopsy the brain showed multiple CMV cranial neuritis, CMV polyradiculitis and CMV ventriculo-ependymitis. While spinal nerve root involvement by CMV may occur in up to 1% of AIDS patients, involvement of cranial nerves is unusual and CMV infection of multiple cranial nerves is distinctly rare.

July 2000: A 70 year old with rigidity, decreased ocular movements, and dementia.

The July Case of the Month (COM): A 70 year old male presented with a four year history of cognitive decline, difficulty expressing himself, and an increasingly unsteady gait with numerous falls. At presentation he was wheel-chair bound. Examination showed some slowing of speech, mild memory impairment, but normal cranial nerves. Spastic weakness and brisk reflexes were also noted, with bilateral ankle clonus. MRI scans were normal. Four years later he was admitted with a urinary tract infection and was mute with severely impaired ocular motility. He died 18 months later and autopsy showed the classic neuropathological findings of typical Progressive supranuclear palsy, including tau-positive glial inclusions.

Fetal akinesia deformation sequence (Pena-Shokeir phenotype) associated with acquired intrauterine brain damage.

An infant with Pena-Shokeir phenotype was born to a cocaine-using mother. The pathologic findings included polyhydramnios, facial anomalies, arthrogryposis, camptodactyly, pulmonary hypoplasia, and tetralogy of Fallot. The neuropathologic findings were diffuse brainstem and spinal cord neuronal degeneration and focal cerebral infarction, consistent with acquired intrauterine ischemic damage.

Spinal dural arteriovenous fistula: the pathology of venous hypertensive myelopathy.

Spinal dural arteriovenous fistulas (SDAVFs) are the most common type of spinal vascular malformation. The arteriovenous shunts, located entirely outside the spinal cord, cause a clinical picture of chronic progressive myelopathy believed to arise from the effects of increased venous pressure and impaired venous drainage on the spinal cord. Despite their well-described clinical and angiographic features, no reports have documented the spinal cord pathology in a case of angiographically or pathologically proven SDAVF. We report such a patient in whom a spinal cord biopsy supported increased venous pressure as a mechanism of neurologic dysfunction.

Experimental demyelination produced by the A59 strain of mouse hepatitis virus.

Intracerebral inoculation of 4- to 6-week-old C57BL/6 mice with the A59 strain of mouse hepatitis virus (MHV), a murine coronavirus, produced biphasic disease. Acute hepatitis and mild meningoencephalitis were followed by subacute spastic paralysis with demyelinating lesions in the brain and spinal cord as determined by Epon-embedded toluidine-blue-stained sections and by electronmicroscopy. MHV-A59 was cultured by plaque assay from the blood, brain, spinal cord, and liver of infected mice during the acute phase, but not in the chronic stage. MHV-A59 antigen was detected by immunofluorescence (IF) until 3 months postinfection (PI). Serum anti-MHV-A59 antibodies were detected from 7 days to 5 months PI. The induction of demyelination by MHV-A59 provides a suitable system to study virus-induced demyelination further.

Gene expression of apolipoprotein(a) within the wall of human aorta and carotid arteries.

Atherosclerosis is associated with arterial deposition of low density lipoprotein (LDL) and lipoprotein(a), Lp(a). Both lipoproteins have been detected in atherosclerotic vessels; however, while LDL has been shown to be only blood-derived, it is not clear whether Lp(a) is also produced within the vessel wall. In the present investigation we studied gene expression of apo(a) and apoB in human blood vessels. Aorta, carotid arteries and liver specimens from 29 adult and pediatric autopsy cases were studied by RT-PCR and Southern blot analysis with primers and probes specific for apo(a), apoB and GAPDH (a control housekeeping gene). The mRNA of apo(a), but not apoB, was found within the vessel wall in both adult atherosclerotic arterial vessels and in pediatric non atherosclerotic vessels. Neither apo(a) nor apoB mRNA was detected in femoral veins. To verify the nature of the detected transcripts, we cloned the 162 base pair (bp) RT-PCR product derived from the arterial wall total RNA. Nucleotide sequencing revealed 100% homology with the apo(a) gene. Thus, while LDL in atherosclerotic arteries is exclusively blood-derived, the accumulation of Lp(a) within the artery may be due in part to in situ production of apo(a) within the vessel wall.

Induction of MHC class I antigens on glial cells is dependent on persistent mouse hepatitis virus infection.

H-2 class I antigens, but not class II antigens, were detected on the surface of glial cells persistently infected with mouse hepatitis virus strain A59 (MHV-A59) as late as 90 days post-infection. Uninfected glial cells remained negative for H-2 class I and class II surface antigens. We have previously shown that conditioned media from infected glial cell cultures (supernatants) contain a factor unrelated to infectious virus and capable of inducing H-2 class I antigens on uninfected glial cells. The synthesis of this factor appears to be dependent on production of infectious virus since the H-2 inducing activity could not be detected 3 days following the addition of neutralizing antibodies to the cultures. This suggests that H-2 inducing activity contains an unstable component, the synthesis of which is dependent on continual virus production. Persistent MHV infection and H-2 class I antigen expression may play a role in MHV-induced demyelination.

Tumor necrosis factor induces expression of MHC class I antigens on mouse astrocytes.

The effect of tumor necrosis factor (TNF) on expression of major histocompatibility complex (MHC) antigens was examined in mouse glial cells in vitro. TNF induced MHC class I, but not class II, antigen expression on the surface of astrocytes but not on oligodendrocytes. Glial cells do not normally express detectable amounts of MHC antigens. Thus TNF may play a role in the immunopathogenesis of neurologic diseases that involve MHC class I-restricted reactions.

Experimental allergic neuritis in the SJL/J mouse: induction of severe and reproducible disease with bovine peripheral nerve myelin and pertussis toxin with or without interleukin-12.

We report a reproducible model of experimental allergic neuritis (EAN) with severe clinical signs and consistent pathological features in mice. Pertussis toxin (PT) in the presence or absence of murine recombinant interleukin-12 (mrIL-12) was used as an adjuvant with bovine peripheral nerve myelin (BPNM) to induce clinical EAN in SJL/J mice. After immunization with a combination of BPNM in complete Freund's adjuvant (CFA) and PT, mice developed severe consistent signs of EAN. The additional treatment of immunized mice with mrIL-12 prolonged the course of EAN characterized by earlier clinical signs of the disease and delayed the recovery stage. Mice injected with BPNM and CFA without PT developed mild clinical signs. Histological examination of the caudae equinae and the sciatic nerves taken from mice with clinical signs of EAN during the recovery stage revealed severe demyelination, remyelination and remnants of mononuclear cell infiltration. Moderate to severe EAN can be induced in SJL/J mice by the injection of a combination of BPNM in CFA and PT. This model can provide a better understanding of mechanism of demyelination in infiltrating peripheral neuropathy.