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Biomedical subjects

M Gallina

Publications and source records attributed to M Gallina.

36 records · Page 2Linked to original sources

Nitrite plasma levels in acute and chronic coronary heart disease.

BACKGROUND: The authors carried out a study on the plasmatic levels of nitrites, which are the sole stable metabolites of nitric oxide (NO), in a group of subjects suffering from various clinical forms of coronary artery disease, aimed at evaluating the endothelial production of NO in acute and chronic ischemic conditions. METHODS: Our series consisted of 104 female subjects (mean age 65 +/- 5) subdivided into: a) 10 subjects with acute coronary heart disease (myocardial infarction); b) 32 with chronic non hypertensive coronary heart disease (CHD); c) 30 with hypertensive CHD (arterial blood pressure over 160/95 mmHg); d) 32 with CHD and hypercholesterolemia (values over 250 mg/dl). Thirty-seven female subjects (mean age 58 +/- 7) without internistic diseases were considered as control subjects. For each sample the plasmatic levels of nitrites were determined by the Gutman and Hollywood method. RESULTS: We discovered that in the patients with chronic coronary heart disease (CHD) the mean value of nitrites was 18 +/- 0.3 mumol/L, not significantly different from the controls (17 +/- 0.5 mumol/L). In the patients with acute CHD the nitrite plasma level were significantly (p < 0.05) higher (30 +/- 2.2 mumol/L) compared to the controls and the patients with chronic CHD. In the group of patients with hypertensive CHD the mean nitrite value was 20 +/- 0.6 mumol/L, significantly (p < 0.05) higher in comparison with the group of non-hypertensive CHD patients (14 +/- 0.3 mumol/L). In the subjects with CHD and hypercholesterolemia the mean value of nitrites was sharply elevated, (25 +/- 1.0 mumol/L), with a highly significant difference (p < 0.01) as compared to the normolipemic CHD patients. CONCLUSIONS: These results lead to the hypothesis that: strong NO production may play a compensatory and protective role during acute myocardial hypoxia; NO defective synthesis may depend on an exhaustive endothelial adjustment in subjects with long-term CHD; a significant increase of the relaxing factor in hypertensive conditions exists; a highly enhanced synthesis of the plasmatic nitrites in hypercholesterolemic patients means an engagement of NO to neutralize the endothelium-damaging molecular substances and particularly the oxided LDL.

Acute Disease↗

Endothelial, haemostatic and haemorheological modifications in migraineurs.

Vasotropic, haemostatic and haemorheological parameters have been investigated in 17 patients suffering from migraine without aura in comparison with 11 sex and age matched healthy control subjects. NO metabolites (NO2- and NO3-), endothelin (ET-1), tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), fibrinogen, D-dimer, fibrinopeptide A, beta thromboglobulin (beta-TG), blood viscosity, plasma viscosity, haematocrit (Htc) and red blood cell (RBC) filterability index (FI) were determined during headache free periods. Migraineurs NO3- and ET-1 plasma levels, compared to control values, showed a significant decrease and increase respectively; fibrinogen, beta-TG and D-dimer appeared slightly lowered in migraineurs, while Htc remained in the normal limits; tPA, PAI-1 and FI were significantly reduced, while fibrinopeptide A, blood viscosity and plasma viscosity at a low shear rate (shr) exhibited a significant rise. Data obtained support the involvement of endothelial, haemostatic and haemorheological functions in the pathogenesis of migraine.

Adult↗

Thrombotic markers during myocardial infarction.

The authors carried out a study on the behavior of some thrombotic molecular "markers" in a group of patients suffering from myocardial infarction, just after the first symptoms and after two weeks from the event. The series consists of 12 subjects (6 males, 6 females, mean age 52 +/- 7), suffering from acute myocardial infarction; just after the first symptoms and instrumental signs (before the thrombolysis) and after two weeks a venous blood withdrawal was done; on the plasma of each sample the determination of fibrinogen (F) (coagulative method), tissue plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), D-dimer (D-D), fibrinopeptide A (FPA) and betathromboglobulin (BTG) (ELISA methods) was performed. The values of t-PA, FPA and BTG did not show remarkable variations; after two weeks from the myocardial infarction compared to the basal values a significant reduction of PAI-1 (4.6 +/- 0.28 UI/ml vs 5.4 +/- 0.33 UI/ml, p < 0.01), D-D (215 +/- 10 ng/ml, vs 253 +/- 12 ng/ml, p < 0.05) and a significant increase of F (294 +/- 28, vs 218 +/- 16 mg%, p < 0.05) were observed. The authors suggest that a basal reduction of the fibrinolytic activity documented by the enhanced PAI-1, may play a major role, influencing pathogenetically the thrombotic event; the other markers seem to be of lower importance, being only secondarily altered in the first phase and gradually returning to a normal pattern after an adequate elapsed time; a preinfarctual hypofibrinolytic condition, probably enhanced by some triggering factor, actually appears the sole prothrombotic system to be counteracted with adequate diet and drug treatments.

Adult↗

Transgenic mice expressing IFN-gamma in the retina develop inflammation of the eye and photoreceptor loss.

PURPOSE: Inflammatory mediators such as interferon-gamma (IFN-gamma) are thought to play a role in ocular disease. Although IFN-gamma was found in the vitreous of mice with experimentally induced autoimmune uveitis, intracameral injection of this cytokine did not induce intraocular inflammation in mice. Therefore, the authors created a transgenic mouse line using the rhodopsin promoter to direct the expression of IFN-gamma in the photoreceptor cells of the retina. These mice, designated rho gamma, enabled them to model intraocular inflammatory disease. METHODS: The authors fused a 2.1 kb 5' Hind III fragment from the murine rhodopsin gene to the IFN-gamma gene and introduced the DNA construct into fertilized zygotes. These were implanted into pseudopregnant C57BL/6 mice, and the resulting progeny were crossed back to balb/c mice. The transgene was identified by Southern blot hybridization. Eyes from the rho gamma mice were either fixed in zinc formalin and stained with hematoxylin and eosin or were frozen in OCT compound and processed for immunostaining using the indirect immunoperoxidase method with DAB as a chromogen. RESULTS: The rho gamma transgenic mice developed intraocular disease, manifested as intraocular cellular infiltration, loss of photoreceptors, corneal clouding, cataract formation, and epithelial and microglial proliferation. Additionally, rho gamma mice exhibited antigenic changes, comprising GFAP expression on Müller cells, accumulation of neurofilament on photoreceptors, and expression of MHC class I and class II molecules on retinal cells. CONCLUSIONS: IFN-gamma alters the antigenic properties of intraocular tissue and induces intraocular inflammation in mice. The results suggest a key position of IFN-gamma in the development of pathologic conditions related to intraocular inflammation and provide a useful animal model for the further study of inflammatory disorders, including autoimmune diseases.

Animals↗

[Determination of antitetanus antibodies. Methodological and epidemiological studies].

We weighed the situation of tetanus immunity in a population sample of the province of Pavia in which both sexes and all age groups were represented. We carried out the survey performing the indirect haemagglutination test with turkey red cells. In each age groups the checked subjects have been classified in three different tetanus antibodies concentration levels: under 0.01 U/ml, between 0.01 and 0.1 U/ml, above 0.1 U/ml. The method we used is easy to perform and has a good reproducibility. The survey points out the good protection against tetanus in age classes under twenty years and the possibility of discovering districts where ineffective immunization methods are performed.

Adolescent↗

[Determination of anti-cytomegalovirus antibodies by the immunoperoxidase method: comparison with the methods of complement fixation and immunofluorescence].

Indirect immunoperoxidase technique (IIP) has been employed for determination of IgG antibody titer to cytomegalovirus (CMV) in sera from 110 blood donors. Titers have been compared with complement fixation (CF) and indirect fluorescent antibody (IFA) technique titers, the latter being applied to determination of all specific antibody classes. Within variability range of the quality of reagents employed in different tests, it seems reasonable to conclude IIP technique is as sensitive as IFA and much more sensitive than CF test. Considering CF test is able to detect only IgG antibody, the advantage of using immunohistochemical techniques is obvious. Moreover IIP does not need fluorescence microscope and results reading is easier and can be delayed. Non-specific staining of Golgi area is shared by both techniques, but endpoint determination has to take into account only the nuclear virus-specific inclusion labelling.

Antibodies, Viral↗

[The immunoperoxidase technic in the rapid identification of human cytomegalovirus on primary isolation].

Immunoperoxidase technique has been applied to the rapid identification of human cytomegalovirus (CMV) strains on primary isolation. Negative and positive results have been constantly confirmed by indirect fluorescent antibody technique (IFA) and by electron microscopy. Using either direct or indirect method it was observed that problems of nonspecific staining of uninfected cells were encountered mostly with direct method, probably because of the lower working dilution of the conjugate (1:20) as compared with higher conjugate dilution used for indirect method (1:150). However, nonspecific cytoplasmic stain of Golgi area of infected cells was observed also with indirect method. Pathogenesis of nonspecific labelling of this area is discussed. Application of the immunoperoxidase technique directly into tubes on primary isolation allows to reduce identification time in comparison with IFA technique and is less cumbersome and time-consuming than complement fixation and neutralization tests.

Antibody Specificity↗

Defect of bone marrow granulocyte reserve in viral hepatitis.

In patients with HBAg-positive and HBAg-negative viral hepatitis the etiocholanolone test showed a decrease of the bone marrow granulocyte reserve at the height and, though at a lower degree, at the end of the disease. These results are discussed in relation with the incidence of aplastic anemia following viral hepatitis.

Adolescent↗

Nitrite plasma levels in type 1 and 2 diabetics with and without complications.

BACKGROUND: The authors thought it interesting to examine the interrelationship between nitric oxide and diabetes mellitus by the determination of the nitrite plasma levels, stable end-products of nitric oxide, in various clinical patterns of diabetes mellitus. METHODS: Our series consisted of 161 female subjects (mean age 54 +/- 7 years, disease duration 5 +/- 3 months) subdivided into: a) 13 patients suffering from insulin-dependent diabetes (IDDM) without clinical and instrumental signs of micro- and macroangiopathy; b) 148 suffering from non insulin-dependent diabetes mellitus (NIDDM) of whom: 1) 52 without vascular complications (28 normal weight, BMI < 25, and 24 obese, BMI > 30); 2) 40 with clinical and instrumental signs of non hypertensive coronary heart disease (CHD); 3) 25 with CHD and hypertension (arterial blood pressure over 160/95 mmHg); 4) 31 with hypercholesterolemia (values over 250 mg/dl). All patients were examined in good glycometabolic conditions reached by oral hypoglycemiant (12 cases) or insulin (149 cases) treatment. As normal control 37 female subjects (mean age 48 +/- 7) without internistic diseases were considered. For each sample we determined the plasma levels of nitrites by the Gutman and Hollywood method. RESULTS: Almost similar nitrite plasma levels in IDDM (17 +/- 0.5 mumol/L) and normal controls (17 +/- 0.2 mumol/L) were found; in non complicated non obese NIDDM a not significantly elevated value (21 +/- 0.8 mumol/L) as compared with the IDDM and control group was found; the obese NIDDM patients showed a value (18 +/- 0.4 mumol/L) not significantly different in comparison with the non obese NIDDM group. In the NIDDM group with non hypertensive CHD) the nitrite value was almost similar (20 +/- 0.5 mumol/L) to the corresponding group without vascular complications. In the patients with CHD and hypertension the nitrite level was superimposable (20 +/- 0.7 mumol/L) on the one recorded in NIDDM patients without vascular complications and in those with CHD without hypertension. In NIDDM patients with hypercholesterolemia the mean nitrite value was sharply elevated (24 +/- 0.8 mumol/L); the difference between this group and those of non hypercholesterolemic, non obese, obese and CHD (with or without hypertension) patients was significant (p < 0.05). CONCLUSIONS: It is conceivable that diabetes mellitus per se causes a tendential not significant increase of NO production in comparison with normal controls; some factors such as blood pressure, overweight, disease duration, therapeutic treatment and coronary complications appear not to influence NO production. In hypercholesterolemic diabetic patients the nitrite enhanced level in plasma might mean a compensatory response to a continuous inactivation of NO involved in a protective competition towards damaging factors and chiefly against oxidised LDL.

Diabetes Mellitus, Type 1↗