Biomedical subjects
Publications and source records attributed to S Bo.
Primary cardiac neoplasms are rare in animals. Hemangiosarcoma is the most common primary cardiac tumour in the dog, but has not been reported in the cat. We describe the clinical signs, the gross examination, and the morphological and immunohistochemical features of a haemangiosarcoma in the right atrium of a 13-year-old domestic shorthair cat. In addition, a distant metastasis was found in the liver.
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AIMS/HYPOTHESIS: The purpose of this study was to investigate the relation between life-style habits and glucose abnormalities in Caucasian women with and without conventional risk factors for gestational diabetes. METHODS: A total of 126 pregnant women with gestational diabetes, 84 with impaired glucose tolerance and 294 with normal glucose tolerance, identified by sequential screening, were interviewed to determine their usual weekly food pattern, amount of exercise, smoking habits and alcohol intake. RESULTS: Patients with glucose abnormalities were older and shorter in height and had significantly higher BMI before pregnancy, percentage of diabetic first-degree relatives and higher intake of saturated fat. Patients without known risk factors for gestational diabetes (i. e. younger than 35 years of age, BMI < 25 kg/m2, no first-degree diabetic relatives) included 40 with impaired glucose tolerance or gestational diabetes. In a multiple logistic regression model age, short stature, familial diabetes, BMI and percentages of saturated fat were associated with impaired glucose tolerance or gestational diabetes in all patients, after adjustment for gestational age. In patients without conventional risk factors only percentages of saturated fat (OR = 2.0; 95 %-CI = 1.2-3.2) and polyunsaturated fat (OR = 0.85; 95 %-CI = 0.77-0.92) were associated with gestational hyperglycaemia, after adjustment for age, gestational age and BMI. CONCLUSION/INTERPRETATION: Saturated fat has an independent role in the development of gestational glucose abnormalities. This role is more important in the absence of conventional risk factors suggesting that glucose abnormalities could be prevented during pregnancy, at least in some groups of women.
BACKGROUND AND DESIGN: Conflicting data exist about uric acid levels in type 2 diabetes mellitus, as low levels were found in diabetic patients, while elevated serum uric acid is a feature of hyperinsulinemia and impaired glucose tolerance. The present study was addressed to evaluate the relation between uric acid and metabolic parameters, creatinine clearance and albumin excretion rate in a cohort of type 2 diabetic patients. RESULTS: Hyperuricemic patients were older and had higher values of body mass index (BMI), systolic and diastolic blood pressure, triglycerides, albumin excretion rate, C-peptide and prevalence of hypertension, metabolic syndrome and macroalbuminuria and lower values of high-density lipoprotein (HDL)-cholesterol, creatinine clearance and glycated haemoglobin (HbA1c). The correlations between uric acid levels and triglycerides, BMI, systolic blood pressure, albumin excretion rate, C-peptide, creatinine clearance, HDL-cholesterol and HbA1c remained significant in a multiple regression analysis after adjustment for age, sex and duration of diabetes. After performing multiple logistic regression analyses, uric acid levels were independently associated with hypertension [odds ratio (OR) = 1.8; 95% confidence interval (CI) 1.6--2], after adjustment for age, sex, duration of diabetes and macroalbuminuria (OR = 1.5; 95% CI 1.1--2.0), after adjustment for age, sex, HbA1c levels, creatinine clearance, duration of diabetes and blood pressure levels and the metabolic syndrome (OR = 1.6; 95% CI 1.5--1.8), after adjustment for age, sex and creatinine clearance. CONCLUSIONS: In type 2 diabetes, hyperuricemia seems to be associated with the insulin-resistant syndrome and with early onset or increased progression to overt nephropathy, while hypouricemia is associated with worse metabolic control, hyperfiltration and a late onset or decreased progression to overt nephropathy.
BACKGROUND: To evaluate if being a twin is a condition at risk of developing metabolic abnormalities in the adult life 'per se' or as a consequence of the lower birth weight. METHODS: 48 monozygotic twins and 50 non-twin controls, both with parental diabetes, were compared; the two groups were comparable for age, sex and body mass index. RESULTS: Twins showed higher values of blood pressure, triglycerides, insulin resistance, fasting insulin, insulin AUCs and higher prevalence of the metabolic syndrome, and, inversely, lower birth weight. After adjustment for birth weight, no significant association was evident with the twin status. Birth weight was inversely associated with the presence of the metabolic syndrome or of at least one or more of its components, while the positive association with the twin status was not significant. CONCLUSIONS: Our data suggest that low birth weight is more relevant than the twin status as a risk factor for the metabolic syndrome and its components.
The relation between isolated low HDL-cholesterol and the components of the metabolic syndrome is poorly known in type 2 diabetes. We evaluated cardiovascular risk parameters in type 2 diabetic patients with low HDL-cholesterol, compared to those with low HDL-cholesterol and hypertriglyceridemia, isolated hypertriglyceridemia and normal lipid parameters. Patients with low HDL-cholesterol/high triglycerides had higher BMI (29.6 +/- 5.7 vs 27.9 +/- 4.4 or vs 28.1 +/- 5.2 kg/m(2) ), prevalence of obesity (69% vs 55% or vs 54%), higher levels of uric acid (339.0 +/- 83.3 vs 303.3 +/- 95.2 or vs 303.3 +/- 89.2 micromol/l) and C-peptide (0.76 +/- 0.40 vs 0.63 +/- 0.33 or vs 0.63 +/- 0.36 nmol/l) and number of components of the metabolic syndrome (27% patients with all the components) compared to patients with isolated low HDL-cholesterol or normal subjects, respectively. A similar pattern of values was evident in patients with isolated hypertriglyceridemia. With logistic regression analysis, BMI and uric acid levels were significantly associated with the presence of hypertriglyceridemia (both isolated or associated with low HDL-cholesterol), while patients with isolated low HDL-cholesterol and those without dyslipidemia displayed a similar more favourable metabolic pattern. These results indicate that low HDL-cholesterol is a component of the metabolic syndrome only in the presence of fasting hypertriglyceridemia in type 2 diabetic patients.
As the relationships between C-peptide levels and metabolic control and chronic complications are poorly known in type 2 diabetes, due to the slow decline of beta-cell function, we evaluated these associations in a cohort of type 2 diabetic patients. After excluding insulin-treated subjects, 1,533 patients were divided according to their C-peptide fasting levels in quartiles. Patients within the lowest C-peptide quartile showed significantly higher duration of diabetes, prevalence of retinopathy and values of HDL-cholesterol, albumin excretion rate and HbA1c, while BMI, diastolic blood pressure, percentages of hypertension and metabolic syndrome, and values of triglycerides and uric acid were significantly higher in the highest C-peptide quartile. The associations between C-peptide and duration of diabetes, AER, HbA1c, retinopathy and the components of the metabolic syndrome remained significant, after multiple adjustments. In conclusion, these data support the hypothesis that a reduced insulin secretion is associated with a longer duration of diabetes and a greater prevalence of microvascular complications, while higher insulin levels are associated with the components of the metabolic syndrome.
An excess of cardiovascular morbidity has been related to low birthweight. The aim of this study was to evaluate the relationship between low birthweight and levels of fibrinogen, lipoprotein(a), and albumin excretion rate, which are known risk factors for coronary artery disease. Seventy-two twins, with the same within-pair gender and normal glucose tolerance, were analyzed in order to avoid confounding factors, such as gestational age, birth order, or sex. Twins with the highest birthweights within the couple showed no significant difference of fibrinogen, lipoprotein(a), and albumin excretion rates compared with the twins with the lowest birthweights among the two co-twins. Moreover, no relevant correlation was found between birthweight and intra-pair birthweight differences and fibrinogen, lipoprotein(a), and albumin excretion rates. The lack of correlation between fibrinogen, lipoprotein(a), albumin excretion rate and birthweight, suggests that these factors do not contribute to the link between intrauterine malnutrition and increased cardiovascular risk.
AIMS: To evaluate the role of environmental intra-uterine factors in determining the birthweights of twins with increased susceptibility to diabetes and discordant for abnormal responses to the oral glucose tolerance test (OGTT) and verify the possible association of within-pair birthweight differences and metabolic abnormalities in adult life. METHODS: Forty-six monozygotic (MZ) and 32 dizygotic (DZ) twins were enrolled; 13 MZ twins were discordant for impaired glucose tolerance (IGT) and/or hyperinsulinaemia compared to their co-twins. RESULTS: The 13 MZ discordant twins showed significantly lower birthweights than their normal co-twins (P < 0.001). When dividing all twins in those with the highest birthweights within the couple and those with the lowest, all subjects with abnormal OGTT were found in the latter group (P < 0.0001). Within-pair birthweight difference was significantly higher in MZ twins with abnormal OGTT and the metabolic syndrome compared to normal MZ twins. The relative risk of developing the metabolic syndrome was 8.7 (1.6-46.9) when comparing the higher tertile of within-pair birthweight differences (> or = 0.450 kg) to the two lower tertiles (< 0.450 kg). Logistic regression analysis confirmed within-pair birthweight difference as a significant predictor of abnormal responses to the OGTT and the metabolic syndrome. CONCLUSIONS: These data suggest a causative role for environmental intrauterine factors on the determination of birthweight and support the hypothesis that within-pair birthweight difference, rather than an absolute low birthweight, is responsible for the metabolic abnormalities in the adult life.
AIMS: To evaluate the roles of maternal and paternal diabetes and diabetes in relatives other than parents on the clinical characteristics in Type 2 diabetes mellitus. METHODS: A total of 2,113 Type 2 diabetic patients were recruited, and those with diabetic mothers, diabetic fathers, diabetic relatives other than parents and no known diabetic relatives, were considered separately. RESULTS: The prevalence of diabetes in the mother, father and other relatives was 25.5, 6.5 and 21.2%, respectively. No difference in the clinical characteristics was found in patients with diabetes in the mother or father. Patients with parental diabetes were significantly younger, with higher LDL-cholesterol, prevalence of retinopathy and lower age at diabetes diagnosis than those without familial diabetes; on multiple logistic regression, only age (P = 0.0003), age at diabetes diagnosis (P = 0.0014) (inverse association), and LDL-cholesterol (P = 0.030) remained significantly associated with parental diabetes. Patients with diabetic relatives other than parents displayed significantly higher total and LDL-cholesterol, prevalence of retinopathy and lower age at diabetes diagnosis that those with no known diabetic relatives; on multiple logistic regression, only age at diabetes diagnosis was inversely associated with diabetes in relatives other than parents (P = 0.013). CONCLUSIONS: The data do not indicate a different influence of maternal and paternal diabetes on the clinical characteristics of Type 2 diabetic patients, while there is evidence that parental diabetes brings to an earlier onset of the disease and higher LDL-cholesterol values; the presence of diabetes in relatives other than parents constituted a small risk for earlier manifestation of the disease.
OBJECTIVE: The increased prevalence of cardiovascular events in type 2-diabetic patients with micro- or macroalbuminuria is not completely explained by an excess of conventional risk factors for atherosclerosis. Genetic polymorphism within the platelet glycoprotein IIIa has been implicated in the etiology of acute coronary syndromes. We tested the hypothesis that the PI(A1/A2) polymorphism could in part account for the increased cardiovascular risk of type 2-diabetic patients with micro- or macroalbuminuria compared to normoalbuminuric diabetic patients. RESEARCH DESIGN AND METHODS: We have examined the PI(A1/A2) polymorphism of the platelet glycoprotein IIIa in type 2-diabetic patients: 94 with micro-, macroalbuminuria, and 94 with normoalbuminuria, matched for age, sex and body mass index. PI(A) genotypes were performed by polymerase chain reaction and restriction enzyme digestion. RESULTS: There was no significant difference in the prevalence of PI(A2)-positive genotypes (either PI(A1/A2) or PI(A2/A2)) in the two groups of patients (chi2 = 0.19, df = 1 , p = 0.66). CONCLUSIONS: These results suggest that carriage of the platelet glycoprotein IIIa PI(A2) allele does not contribute to explain the increased cardiovascular risk associated with micro- or macroalbuminuria in type 2 diabetes.
OBJECTIVE: To study the clinical therapeutic effect of Shenning Mixture (SNM) in treating IgA nephropathy. METHODS: Patients were treated separately with SNM or prednisone by randomized grouping. The criteria, including clinical symptoms, signs, hematuria, albuminuria and immune globulin were observed. RESULTS: The total effective rate and the complete remission rate in the SNM group were 97.1% and 45.7% respectively, while in the control group, they were 37.1% and 8.6% respectively. Comparison of the two groups showed that the therapeutic effect in the former was better than that in the latter significantly, P < 0.01. The hematuria and albuminuria extenuated and serum IgA lowered more significantly in the SNM group than those in the control group (P < 0.05, P < 0.01). CONCLUSION: SNM has obvious therapeutic effect on the hematuria and albuminuria in treating IgA nephropathy.
There are contrasting data about the relationship between obesity and macrovascular complications in type 2 diabetes mellitus, and it is not known if risk factors for coronary artery disease are different in normal weight and overweight or obese patients. All 2113 patients with type 2 diabetes mellitus referring to the Diabetic Clinic of Asti were studied. Patients were divided into tertiles of body mass index, according to their sex (BMI < 26.9; >/= 26.9 and < 31.4; >/= 31.4 kg/m(2) for females and BMI < 25.7; >/= 25.7 and < 28.8; >/= 28.8 kg/m(2) for males). Age, BMI, duration of diabetes, blood pressure, HbA(1c) total cholesterol, HDL-cholesterol, LDL-cholesterol, and prevalence of insulin treatment and hypertension were higher in females, whereas exercise, alcohol intake, smoking habits and prevalence of dyslipidemia were higher in males. An increase in BMI was associated with an increase in HbA(1c), number of cigarettes/day, blood pressure, triglycerides, C-peptide, prevalence of hypertension and dyslipidemia, and with a decrease in age, duration of diabetes and HDL-cholesterol values. In spite of an apparently worse cardiovascular risk profile, females showed a 50% lower prevalence of CAD than males and the prevalence of CAD was not significantly different in obese compared to other BMI categories. Multiple logistic regression showed that risk factors for CAD were different in males and females and similar in the lower tertiles of BMI, while different in the highest. In obese females, risk factors for CAD were age, reduced HDL-cholesterol and increased HbA(1c) levels; in males they were years of smoking and duration of diabetes. These data suggest that in type 2 diabetes, risk factors for CAD are different in the two sexes and in patients with the highest BMI compared to the normal and overweight subjects; blood glucose control and duration of diabetes seem more important than conventional cardiovascular risk factors in obese patients.
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A 7-month-old Korat cat was referred for a slowly progressive neurological disease. Circulating monocytes and lymphocytes showed the presence of single or multiple empty vacuoles and blood leukocytes enzyme assay revealed a very low beta-galactosidase activity level (4.7 nmol/mg per h) as compared to unaffected parents and relatives. Histologically, the cat, euthanized at the owner request at 21 months of age, presented diffuse vacuolization and enlargement of neurons throughout the brain, spinal cord and peripheral ganglia, severe cerebellar neuronal cell loss, and moderate astrocytosis. Stored material was stained with periodic acid-Schiff on frozen sections and with the lectins Ricinus conmmunis agglutinin-I, concanavalin A and wheat germ agglutinin on paraffin-embedded sections. Ultrastructurally, neuronal vacuoles were filled with concentrically whorled lamellae and small membrane-bound vesicles. In the affected cat, beta-galactosidase activity was markedly reduced in brain (18.9%) and liver (33.25%), while total beta-hexosaminidase activity showed a remarkable increase. Quantitation of total gangliosides revealed a 3-fold increase in brain and 1.7-fold in liver of affected cat. High-performance thin layer chromatography (HPTLC) detected a striking increase of GM1-ganglioside. On densitometric analysis of HPTLC bands, the absorption of GM1-ganglioside band was 98.52% of all stained bands (GD1a, GD1b, GT1b). Based on clinical onset, morphological and histochemical features, and biochemical findings, the Korat cat GM1-gangliosidosis is comparable with the human type II (juvenile) form. However, clinical progression, survival time and level of beta-galactosidase deficiency do not completely fit with those of human type II GM1-gangliosidosis. The disease in the Korat cat is also different from other reported forms of feline GM1-gangliosidosis.
Cerebrospinal fluid (CSF) obtained from 20 clinically healthy dogs and from 15 dogs affected by neurological disorders were examined for total and differential cell counts, immunocytochemistry for canine distemper virus antigen, total protein concentration and electrophoretic separation, and glucose and enzyme determination. Dogs affected by canine distemper showed an increase in macrophages, presence of specific inclusion bodies, and an increase in total protein concentration and gamma-globulin fraction. In bacterial meningoencephalomyelitis pleocytosis, increase of total proteins with special regard to high molecular weight proteins, elevated levels of lactate dehydrogenase (LDH), alterations of LDH isoenzyme profile, and decrease in glucose levels were detected; inflammatory disorders were more often characterized by an increase in LDH level, while in non-inflammatory disorders (hydrocephalus and spinal cord neoplasia) no variation in LDH levels was detected. Analysis of CSF in dogs appears relatively easy to perform and may help in establishing the condition of the blood-brain barrier as well as in the diagnosis of neurological disorders.
To evaluate the inheritance of cardiovascular risk parameters in subjects with increased susceptibility for non-insulin-dependent diabetes mellitus, we compared 25 pairs of healthy twins who were offspring of diabetic parents with 25 pairs without a parental history for type 2 diabetes mellitus (12 monozygotic and 13 dizygotic in each group). Environmental factors were also evaluated to avoid bias in the assessment of concordance. No significant difference was found in concordance between monozygotic and dizygotic twins for physical activity, diet, smoking, alcohol intake and living together or apart. Genetic analysis revealed a substantial heritability for weight, body mass index, percentage of body fat, lipoprotein(a), high density lipoprotein (HDL)- and HDL2-cholesterol, without significant differences between the two groups. We conclude that heritability of several cardiovascular risk parameters is not increased in subjects with increased susceptibility to type 2 diabetes mellitus.
Neuropathological examination of the central nervous system of 13 naturally and 13 experimentally feline immunodeficiency virus (FIV)-infected cats revealed diffuse gliosis of gray and white matter and vacuolar myelinopathy in a large proportion of infected animals, sometimes associated with lymphocytic meningitis. Multinucleated giant cell formation, the hallmark of multifocal giant cell encephalitis in HIV infection, was never observed. Morphometric analysis confirmed a marked increase of GFAP reactivity in infected cats. Gliosis was mainly present in cortical structures of frontal, parietal, and occipital lobes. Only one naturally infected animal evidenced clinical symptoms of neurological damage. This study confirms that FIV provides an interesting model for studying HIV-induced cortical and subcortical brain pathology believed to be the cause of the neurological manifestations frequently observed in AIDS patients.