Parenchymal Forms Research Articles

Maternal hypothyroxinemia influences glucose transporter expression in fetal brain and placenta.

The influence of maternal hypothyroxinemia on the expression of the glucose transporters, GLUT1 and GLUT3, in rat fetal brain and placenta was investigated. Fetal growth was retarded in hypothyroxinemic pregnancies, but only before the onset of fetal thyroid hormone synthesis. Placental weights were normal, but placental total protein concentration was reduced at 19 days gestation (dg). Immunoblotting revealed a decreased abundance of GLUT1 in placental microsomes at 16 dg, whereas GLUT3 was increased. Fetal serum glucose levels were reduced at 16 dg. In fetal brain, the concentration of microsomal protein was deficient at 16 dg and the abundance of parenchymal forms of GLUT1 was further depressed, whereas GLUT3 was unaffected. Northern hybridization analysis demonstrated normal GLUT1 mRNA levels in placenta and fetal brain. In conclusion, maternal hypothyroxinemia results in fetal growth retardation and impaired brain development before the onset of fetal thyroid function. Glucose uptake in fetal brain parenchyma may be compromised directly, due to deficient GLUT1 expression in this tissue, and indirectly, as a result of reduced placental GLUT1 expression. Though corrected by the onset of fetal thyroid hormone synthesis, these deficits are present during the critical period of neuroblast proliferation and may contribute to long term changes in brain development and function seen in this model and in the progeny of hypothyroxinemic women.

CENTRAL NERVOUS SYSTEM TUBERCULOSIS

Involvement of the central nervous system (CNS) by Mycobacterium tuberculosis, particularly meningitis, is the most severe form of tuberculous infection. Parenchymal CNS involvement can occur in the form of tuberculoma or, more rarely, abscess. Although surgery was initially advocated as the mainstay of therapy, more recent evidence suggests that parenchymal forms of CNS tuberculosis can be cured with medical treatment alone. Also, damage of the spinal cord, roots, and spine can occur in the form of spinal meningitis, radiculomyelitis, spondylitis, or spinal cord infarction.

Recent Developments in the Epidemiology, Diagnosis, Treatment, and Prevention of Neurocysticercosis.

Neuroimaging studies have revealed that neurocysticercosis is a major cause of neurologic disease in most developing countries and is an emerging disease in industrialized areas. Patients with neurocysticercosis present mainly with seizures (parenchymal form) or intracranial hypertension (ventricular/subarachnoid forms). Management should be based on a thorough understanding of the pathogenesis and natural history of infection. Symptoms of active parenchymal neurocysticercosis result from the host inflammatory response to the dying metacestode form. Careful use of anticonvulsants will result in an excellent clinical outcome. The anthelminthic drugs albendazole and praziquantel are effective in killing the cysts, but their long-term effect on prognosis is unproven. Patients with obstructive hydrocephalus from ventricular cysts should be managed surgically by cerebrospinal fluid diversion or cyst removal. Treatment with antiparasitic drugs (especially albendazole) and corticosteroids may decrease the incidence of shunt failure. Current efforts at control of the disease include mass human or porcine chemotherapy in endemic zones and vaccination.

MRI of CNS parasitic diseases.

This article reviews MRI findings of parasitic diseases of the central nervous system (CNS), with emphasis on neurocysticercosis, which is by far the most common CNS parasitic infection worldwide. MRI findings of neurocysticercosis are various, depending on the location (parenchymal, cisternal, ventricular, and spinal forms), and temporal evolutional stages (vesicular, colloid vesicular, granular nodular, and nodular calcified stages) of the worm. Classical findings of each location and stage are presented. Characteristic MRI findings of cerebral toxoplasmosis frequently seen in patients with acquired immunodeficiency syndrome (AIDS), paragonimiasis, and sparganosis that have most commonly been reported in East Asia are also illustrated. MRI is superior to CT scan in the evaluation of most CNS parasitic infections and is nearly diagnostic, particularly in endemic areas. Contrast-enhanced study is essential not only for specific diagnosis of the disease, but also for assessment of the inflammatory activity.

Successful hormonal treatment of pulmonary parenchymal endometriosis

Endornetriosis usually remains localized to the peritoneal cavity and intrathoracic endometriosis, in both its pleural and parenchymal forms, is very rare [l]. It can manifest as catamenial pneumothorax, catamenial hemoptysis, or an asymptomatic pulmonary nodule. The catamenial occurrence of symptoms is highly typical and is the most important diagnostic indicator. There is limited information available regarding the management of this disorder. We report a woman with catamenial hemoptysis which was diagnosed clinically and treated successfully with a gonadotropin-releasing hormone analogue followed by danazol. A 31-year-old Japanese woman (gravida 0, para 0) was admitted to our hospital after three episodes of hemoptysis over 3 months, all at the

Brain parenchymal and microvascular amyloid in Alzheimer's disease.

Brains of patients with Alzheimer disease/senile dementia of Alzheimer type (AD/SDAT) develop a progressive accumulation of amyloid, which deposits primarily in the form of characteristic parenchymal 'plaques' (senile or neuritic plaques/SP's) and as mural deposits in the walls of capillaries and arterioles (cerebral amyloid angiopathy /CAA). A major component of this amyloid is a small and unique peptide composed of 39-43 amino acids, beta/A4, which is cleaved from a much larger precursor protein (APP) that has several isoforms. Brain amyloid can be detected in autopsy or biopsy brain tissue by classical, immunohistochemical and ultrastructural (including immuno-electron microscopic) methods of varying sensitivity and specificity. Beta/A4 amyloid deposition is remarkably variable (e.g. predominantly parenchymal or vascular, or a mixture of parenchymal and vascular) among patients with AD/SDAT. Despite its abundance in the brains of AD/SDAT patients, the precise role of beta/A4 in the pathogenesis of the neurological deficit, neocortical atrophy and progressive synapse loss associated with AD/SDAT has yet to be determined. However, mutations in the gene that encodes APP are clearly associated with familial AD syndromes in which there is significant brain amyloid deposition. CAA, in addition to its association with AD/SDAT, can result in hemorrhagic and (possibly) ischemic forms of stroke. Work with recently developed transgenic mice which express large amounts of beta/A4 in the central nervous system is likely to elucidate mechanisms by which the protein is selectively or deposited in the brain in a parenchymal or microvascular form, and how it contributes to the pathogenesis of neurodegeneration.

Parenchymal-stromal interactions in neoplasia. Theoretical considerations and observations in melanocytic neoplasia.

The paper briefly reviews the reciprocal and continuous reciprocal interactions between epithelia, mesenchyme, and extracellular matrix in the development and maintenance of organismal form in multicellular organisms in the animal kingdom and describes the progressive changes in parenchymalstromal interactions in melanocytic neoplastic development and progression. In addition to the parenchymal stromal form in non-lesional skin seven different and unique stromal patterns are described. These have been termed: 1) The stroma (diff-regress) of programmed differentiation leading to lesional regression characteristic of common nevi; 2) concentric eosinophilic fibroplasia (cef), the hallmark of precursor nevi (dyplastic nevi) with and without melanocytic nuclear atypia; 3) Fibroplasia with angiogenesis (fa) commonly seen in superficial spreading melanoma without metastic competence (SSM); 4) Lamellar fibroplasia (lf) seen in precursor nevi and melanomas with and without metastatic competence; 5) Diffuse fibroplasia with angiogenesis (dfa), 6) Narrow, uniform concentric eosinophilic fibroplasia (nucef), 7) No parenchymal-stromal interaction (nopsi); the last three being seen in the heterogeneous stroma of melanomas of the superficial spreading type with metastatic competence. The changes in neoplastic stroma proceed in concert with the changes in the parenchyma characteristic of melanocytic tumor progression.

Computed tomography of intracranial tuberculosis

The many clinico-radiological manifestations of intracranial tuberculosis have been well documented; however, few long-term retrospective serial studies of large series of patients on therapy have been reported utilizing computed imaging. The computed tomographic appearance, sequential periodic evolution, and final outcome of all patients with cranial tuberculosis seen at this institution in a period of ten years have been evaluated. A total of 80 subjects with intracranial tuberculosis revealed 17.5% with Type I isolated meningeal involvement, 71.25% with Type II isolated parenchymal forms, and 11.25% with Type III compound parenchymal/meningeal lesions. Only 28.8% had concomitant manifestations of TB outside the CNS. Seventy four of these patients were followed on medical or combined medical/surgical therapy which demonstrated 24.3% (n = 18) resolution without radiographic sequellae, 66.2% (n = 49) resolution with residual stroke, atrophy and/or calcification, and 4.1% (n = 3) with persistent enhancement of the lesion(s) after two years of treatment. Four deaths occurred all of which were in patients with Type III TB. This large group of patients followed from presentation to radiologic resolution of the disease process by computed tomography yields important information on the presentation, prognosis and sequelae of intracranial tuberculosis.

Solitary bronchial amyloid presenting with haemoptysis

Pulmonary amyloidosis can be classified into tracheobronchial diffuse alveolar-septal and nodular parenchymal forms. Tracheobronchial amyloidosis can be further subdivided into diffuse and focal varieties. The latter is rare. We report a patient with a focal intrabronchial deposit of amyloid who presented with haemoptysis. The haemoptysis ceased following bronchoscopic removal of this deposit.