The effect of education and self-monitoring of blood glucose on glycosylated hemoglobin in type I diabetes. A controlled 18-month trial in a representative population

The influence on glycosylated hemoglobin (HbA1) of formal education as compared with self-monitoring of blood glucose (SMBG) was studied in a randomized 18-month trial. All adult type I diabetics in a community were identified. Forty-one of these patients had had diabetes for 20 years or less. Thirty-seven patients were included in the study and finally randomized into four groups. Ten patients received individual formal education followed by SMBG, eight patients were instructed in SMBG without pre-education, nine patients were given only formal education and 10 patients made up a reference group. Education did not improve the mean HbA1 values. SMBG resulted in a decrease by 2% in HbA1, from 12 to 10% (p less than 0.05). The final HbA1 level, however, did not differ significantly between any of the groups. SMBG was accepted by 80% of the patients. The liability to hypoglycemia was about equal in the four groups. It was concluded that SMBG, but not education, improved metabolic control to a certain degree.     

Masking,De Lange curves and integration time as revealed by the electroretinogram of a tree shrew (Tupaia chinensis)

In order to elucidate the effects of angiotensin II on renal function, angiotensin II (AII; 1 ng/kg per min) and the AII antagonist 1-sar-8-ala-angiotensin II (AIIA; 200 ng/kg per min) were infused into the renal artery of anesthetized dogs (pentobarbital), on either a high (8 mmol/kg per day for seven days) or a low sodium intake (0.5 mmol/kg). In sodium replete dogs AII produced renal vasoconstriction with decreased RBF (–28%;P<0.001), but with less decrease of GFR (–14%;P<0.001), leading to an increase of FF (+19%;P<0.01),andantidiuresis(–39%;P<0.001); the antinatriuresis (–58%;P<0.001) exceeded the antidiuresis (P<0.001). RBF (–10%;P<0.001) was less pronounced (P<0.001) during AII in sodium deplete dogs, GFR remained unchanged, but FF increased to the same extent (+16%;P<0.05); diuresis and urinary electrolyte excretion were however not affected. AIIA did not affect RBF, GFR, FF, nor diuresis in sodium replete dogs suggesting that endogenous AII has no tonic influence on renal function in these conditions. In sodium deplete animals AIIA produced an 11% (P<0.001) increase of RBF, without changes of GFR; FF decreased by 12% (P<0.01), but diuresis, natriuresis and kaliuresis were not affected.     

Striated muscle ultrastructure in intermittent claudication

Twenty-four biopsy specimens from the lower leg muscles of 21 patients with intermittent claudication were studied by electron microscopy. Sixteen of the specimens contained hypertrophic, atrophic, autolytic, or phagocytic fibers, or other forms of macroscopic fiber degeneration. Of the pathological changes in the cell organelles, the most common was simple myofibrillar degeneration, followed by slightly pathological mitochondria and excessive accumulations of glycogen and lipofuscin. Different types of basement membrane alterations and central nuclei were present in 16 of the biopsy specimens. Most of the pathological changes were the same as those previously reported by others to occur in specific diseases of muscle. There was some positive correlation of the degree of pathological changes to the estimated clinical severity of claudication.     

Malaria of importation in the child: epidemiological, clinical and therapeutic analysis. Apropos of 70 cases observed in a pediatric hospital in Paris

Seventy children from 7 months to 15 years old have been treated for malaria at Hospital Trousseau (Paris) during years 1987 and 1988. Thirty nine of them were living in France usually. The infection was one chiefly in Africa (68 cases), and by P. falciparum in 78% of children. The digestive symptoms were frequent (40/70); splenomegaly was observed in 40 children and hepatomegaly in 31. Anemia was present in 59 cases and mild thrombopenia for 31 cases. The C. reactive protein raised in 92% of cases. The diagnosis was late in 31 patients. Only one cerebral malaria case was observed. The chemoprophylaxis was unfitted or absent in 74% of children living in Paris. The chloroquino-resistance was clinically present in 17 cases and the mefloquine was more often used during 1988 year.     

Age-related progression of tau pathology in brains of baboons

Recently, cytoskeletal changes associated with abnormally phosphorylated tau protein were demonstrated in neurons and glial cells of two aged baboons (Papio). The present study examines the effects of age on the development of tau pathology in baboons. Brains of 50 baboons ranging in age from 1 to 30 years were categorized into four age groups: Group I: 1–10 years [n = 9], group II: 11–20 years [n = 13], group III: 21–25 years [n = 17], group IV: 26–30 years [n = 11]). Whole hemisphere sections (100 μm) were examined using phosphorylation-dependent anti-tau antibodies. Cytoskeletal changes were completely absent in animals of group I. In group II four animals (31%) exhibited cytoskeletal changes which were rated as mild or moderate. In group III abnormal tau was found in 12 brains (71%) ranging in severity from mild to severe. Finally, in group IV 10 out of 11 animals (91%) exhibited some degree of tau pathology which was rated as severe in 4 animals (36%). A statistically significant relationship was found between advancing age and progression of tau pathology in baboons. In conclusion, the present findings underline the value of the baboon as a potential nonhuman primate model for age-related tau pathology afflicting the human brain.     

Cell-surface ganglioside GD2 in the immunohistochemical detection and differential diagnosis of neuroblastoma.

The expression of the disialoganglioside GD2 was analyzed in 67 solid tumors and normal tissues from children by using the GD2-specific murine monoclonal antibody 3A7 and the indirect immunoperoxidase method. GD2 was expressed in all of 28 neuroblastomas and was most abundant in stroma-poor tumors. In differentiating stroma-rich neuroblastomas, neuroblastic clusters, neurofibrils, and most ganglion-like cells were positive, whereas Schwann's-cell stroma did not express GD2. In ganglioneuromas, only a few ganglion-like cells showed GD2, whereas all other structures were negative. Scattered foci of ganglioside GD2 also were found in some non-neuronal tumors, such as rhabdomyosarcomas and osteosarcomas, but not in lymphomas, Askin tumors, or most Wilms' tumors. The monoclonal antibody 3A7 is a useful aid in the immunohistochemical diagnosis of neuroblastoma. In addition, the intense cell surface staining of neuroblastoma cells by this reagent makes it potentially useful for detecting residual neuroblastoma in bone marrow samples and lymph node biopsies.     

Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex

Summary Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre- of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.     

Relationship between clinical and radiological diagnostic criteria for Alzheimer's disease and the extent of neuropathology as reflected by 'stages': a prospective study

The distribution of pathology related to Alzheimer's disease (AD) is not uniform throughout the brain. Sites which have a predilection for the development of Alzheimer-type pathology are the limbic regions and neocortical association areas. The changes in these areas of the brain develop gradually, following a well-determined sequence that allows a pathological staging of the disease process. According to the staging hypothesis, the first pathological alterations develop in the transentorhinal and entorhinal regions. The neurofibrillary pathology then spreads into the hippocampus, but not until the final stages does it affect the neocortex. In this study we analyse the relationship between the pathological stages of AD, according ot the staging hypothesis, and the clinical diagnosis in a prospectively assessed patient group. Prediction of any given pathological stage from the clinical diagnosis was found to be poor. This may be partly due to the fact that additional pathologies can alter the clinical picture and severity of dementia in patients who are only in the initial stages of AD. Nevertheless, the NINCDS-ADRDA clinical criteria had a high sensitivity for detection of AD-related pathology: the 'probable AD' category included 22/38 (57.9%) of those in the late isocortical stage, while the 'possible AD' category included 19/23 (82.6%) of those in the limbic stage. Using proposed neuro-imaging protocols for improved identification of patients with AD-related pathology, we largely identified subjects in whom the extent of pathology had spread to the neocortex.