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Biomedical subjects

J Mattila

Publications and source records attributed to J Mattila.

At least 73 records · Page 4Linked to original sources
PubMed1987

Tumour DNA ploidy as an independent prognostic factor in breast cancer.

We determined nuclear DNA content from 308 archival paraffin-embedded malignant breast tumours and evaluated the survival of the patients by univariate and multivariate statistical analyses. The overall 8-year survival rate of stage I-III breast cancer patients was 74.3% in DNA-diploid and 51.2% in DNA-aneuploid tumours (P less than 0.0001). DNA ploidy had prognostic significance in both node-negative and node-positive breast cancer, primarily in cases with steroid receptor-positive tumours. In a Cox multivariate analysis DNA ploidy (P = 0.001), primary tumour size (P = 0.0007), nodal status (P = 0.04) and the content of progesterone receptors (P = 0.0008) emerged as significant independent prognostic factors, whereas oestrogen receptor status, age and menopausal status of the patients had no significant independent prognostic value. If the histological grade of ductal carcinomas was also included in the Cox model, both grade and DNA ploidy had independent prognostic effect. In conclusion, our results indicate that the analysis of DNA ploidy is a useful adjunct in the assessment of prognosis for breast cancer patients.

Aged↗
PubMed1987

Trimethoprim and sulfadiazine penetration into bile and gallbladder in acute cholecystitis.

The concentrations of trimethoprim (TMP) and sulfadiazine (SDZ) in serum, bile and gallbladder wall of 9 patients with acute cholecystitis were measured after b.i.d. treatment with 160 mg of TMP + 500 mg of SDZ. The samples were collected 2-4 h after the last dose. Mean TMP concentrations were 1.71 +/- (SE) 0.51 micrograms/ml, 4.53 +/- 5.26 micrograms/ml and 2.31 +/- micrograms/g in serum, bile and gallbladder, respectively. Mean SDZ concentrations were 22.2 +/- 14.9 micrograms/ml in serum, 9.37 +/- 8.99 micrograms/ml in bile and 16.1 +/- 10.1 micrograms/g in gallbladder. The average ratios of bile-serum and gallbladder-serum concentrations were 2.64 and 1.35 for TMP and 0.42 and 0.73 for SDZ. There was a significant correlation between serum and gallbladder concentrations of both TMP and SDZ. No correlation existed between serum and bile levels.

Acute Disease↗
PubMed1986

Sympathomimetic pressor responses to thyrotropin-releasing hormone in rats.

Cardiovascular responses to centrally administered thyrotropin-releasing hormone (TRH) were studied in urethan-anesthetized rats to allow continuous recording of attendant changes in sympathetic nerve activity. Intracerebroventricular infusions of TRH (0.05-5.0 micrograms) consistently increased not only blood pressure and heart rate, but also spike frequency in splanchnic, renal, or cervical sympathetic nerves. Parasympathetic inhibition seemed unlikely because TRH responses were unaltered by cholinergic blockade with atropine, and efferent vagal nerve firing, instead of being reduced, was actually increased by TRH. An increased secretion of endogenous vasopressin also appeared unlikely, since TRH responses were essentially unaffected by either hypophysectomy or pretreatment with a vasopressin antagonist. Inasmuch as pharmacological ganglion blockade with pentolinium eliminated increases in splanchnic nerve firing but reduced the attendant tachycardia by only 50%, residual tachycardia after ganglion blockade was considered partly due to persistent sympathetic cardioaccelerator tone. On the other hand, because pressor responses to TRH were always accompanied by increased sympathetic nerve firing and were completely abolished after pentolinium-induced ganglioplegia, they were attributed solely to sympathetic hyperactivity.

Animals↗
PubMed1986

Bleeding of a venous hemangioma inside the filum terminale.

Spinal vascular malformations can present with acute symptoms suggesting spinal cord or nerve root compression. We describe a case of bleeding from a venous hemangioma within the filum terminale. This malformation caused acute compression of the lumbar spinal roots. Thus, vascular malformations may exist behind the symptoms of acute radiating pain and lower extremity weakness. They can be treated by total extirpation, when possible, by resection or by decompressive laminectomy alone.

Cauda Equina↗
PubMed1986

Sympathetic vasoconstriction and renin secretion cause pressor responses to thyrotropin-releasing hormone in rats.

To study peripheral mechanisms underlying cardiovascular responses to thyrotropin-releasing hormone (TRH) we recorded the effects of i.c.v. infusions of TRH in urethane-anesthetized rats after various drug pretreatments, nephrectomy or renal denervation. TRH invariably increased blood pressure, heart rate and sympathetic nerve activity. After alpha-1 adrenergic blockade with prazosin, pressor responses to TRH were delayed in onset and reduced in magnitude. After renal denervation or pretreatment with propranolol for beta adrenergic blockade, captopril for converting enzyme inhibition or Sar1Ile8 angiotensin II for angiotensin II blockade, pressor responses to TRH were unaltered during the first few minutes but became significantly reduced thereafter. Bilateral nephrectomy inhibited markedly the whole pressor response including its onset and subsequent elevation. Consequently, initial inhibition by prazosin was considered due to removal of alpha-1 adrenergic vasoconstriction whereas the later attenuation was attributed to antagonism of the renin-angiotensin system. None of the procedures tested affected the attendant sympathetic hyperactivity, but the tachycardia was prevented by beta adrenergic blockade. These results are compatible with the interpretation that, by acting centrally, TRH stimulates sympathetic hyperactivity which then elevates blood pressure by increasing not only sympathetic vasomotor tone but also renal renin secretion.

Angiotensin II↗
PubMed1985

Studies on the site and mechanism of the inhibitory action of intracerebral histamine on the cold-stimulated thyrotropin secretion in male rats.

The locus of the inhibitory action of histamine on cold-stimulated TSH secretion was studied in male rats. Various histaminergic drugs were given either into the median eminence (ME), the third ventricle, the rostral and caudal part of anterior hypothalamus (rAH and cAH) or the posterior hypothalamus (PH) of conscious rats. When infused into ME, histamine (5 and 10 micrograms/rat) decreased and mepyramine (2.5 micrograms) increased the cold-stimulated TSH secretion while a larger dose of mepyramine (10 micrograms/rat), impromidine (0.05 and 0.1 microgram/rat), 2-pyridylethylamine (2-PEA; 5 and 10 micrograms/rat) and cimetidine (2.5 and 7.5 micrograms/rat) had no effect. The inhibitory action of histamine (5 micrograms/rat) was most marked 30 min after the infusion into ME and it remained significant for at least 50 min. Neither cimetidine (50 and 100 mg/kg i.p.) nor mepyramine (10 and 20 mg/kg i.p.) antagonized the inhibitory action of histamine (5 micrograms/rat) in ME. Histamine (10 micrograms/side) inhibited the cold-stimulated TSH secretion likewise when infused bilaterally either into rAH, cAH or PH. TSH secretion induced by exogenous TRH (100 ng i.p.) was also inhibited by histamine (1 microgram/rat) given into the third ventricle. In conclusion, histamine seems to have an inhibitory action on the cold-stimulated TSH secretion. This action is apparently mediated through areas close to the third ventricle. The mechanism of this action seems to be fairly non-specific, i.e. it is mediated through neither H1- nor H2-receptors.

Animals↗
PubMed1985

The effect of maneb, zineb, and ethylenethiourea on the humoral activity of the pituitary-thyroid axis in rat.

Ethylenebisdithiocarbamates (EBDCs) maneb and zineb are widely used fungicides the final metabolite of which is ethylenethiourea (ETU). EBDCs distort the humoral activity of the thyroid gland, and ETU is especially active in this respect. Male Wistar rats were exposed either to exogenous (100 ng i.p.) or endogenous (+4 degrees C) TRH stimulation. ETU (100-500 mg/kg i.p.) caused no changes in serum TSH levels whereas zineb (70-500 mg/kg i.p.) significantly decreased the bursts induced by cold or exogenous TRH. Maneb (20-200 mg/kg i.p.) significantly decreased the cold-induced TSH response while it had no effect on the TRH-stimulated TSH secretion. None of the agents caused significant changes in serum T3 or T4 levels. It seems that maneb, and zineb, but not ETU, inhibit rat TSH secretion through an action on the endogenous TRH at the hypothalamic or pituitary level. The mechanism behind this action may be the inhibition of dopamine-beta-hydroxylase.

Animals↗
PubMed1985

Status of the toxicity reports of pesticides for their registration in Finland.

Recently, attention has centered on the validity of toxicity reports for the registration of pesticides. In Finland, a study was conducted to evaluate the validity of the toxicity reports of pesticides done in U. S. laboratories. Twenty-seven pesticide formulations of the 230 on the market in Finland were selected for the study. The material contained 61 toxicity reports of 16 pesticide formulations done in U. S. laboratories considered questionable, 64 reports from U. S. laboratories considered reliable, and 142 reports originating from European laboratories, totally 267 reports. These reports were divided into valid according to the Organization for Economic Cooperation and Development (OECD) guidelines, and included those with minor discrepancies but in compliance with the good laboratory practice at the time of the study (group I), and and invalid according to the OECD guidelines (group II). After a closer evaluation of the 125 U. S. reports, 85 reports were considered valid and 40 invalid. As a function of time, the proportion of valid studies of all studies on pesticides for the registration purposes in Finland increased during 1961-1981 from 47 to 93%, being 100% at the present time. The lack of information of pesticide formulations registered earlier creates a problem to be solved in the future in Finland, rather than the lack of the validity of toxicity reports.

Animals↗
PubMed1985

Prophylaxis and treatment of anaerobic infections following caesarean section with tinidazole.

The purpose of this prospective, double-blind, placebo-controlled study was to clarify the effect of a single intravenous infusion of 500 mg of tinidazole on infections that followed a caesarean section. 80 consecutive caesarean-section patients and thereafter 72 women undergoing non-elective caesarean section were randomly assigned to two groups, each receiving intravenous infusions at cord clamping. In the entire sample the incidence of endometritis/wound infection in the placebo group was 27.3% (21/77) versus 10.7% (8/75) in the tinidazole group (p less than 0.01). In the non-elective caesarean-section group the incidence of endometritis/wound infection was 39.6% (21/53) in the placebo group versus 14.3% (7/49) in the tinidazole group (p less than 0.01). 27 positive bacterial cultures yielded a pure anaerobic growth in 59% (16/27) of cases, of which 87.5% (14/16) were treated successfully with oral tinidazole.

Adult↗
PubMed1984

Dual action of morphine on cold-stimulated thyrotropin secretion in male rats.

The effect of morphine infused into 4 hypothalamic locations and the periaqueductal gray (PAG) on cold-stimulated thyrotropin (TSH) secretion was studied in male rats. Morphine decreased TSH cold-response when infused into the 3rd ventricle (1-20 micrograms/rat) or the median eminence (5 and 10 micrograms/rat). Infusions bilaterally into the anterior hypothalamus (1-10 micrograms/side) or PAG (1 and 10 micrograms/rat) were ineffective, while those given into the posterior hypothalamus (1 and 5 micrograms/side, but not 10 micrograms/side) significantly enhanced TSH cold-response. Naloxone pretreatment (2 or 5 mg/kg, s.c.) reversed the decreasing effect of morphine in the 3rd ventricle (1 microgram/rat) and the increasing effect of morphine in the posterior hypothalamus (1 microgram/side). We conclude that morphine has a dual hypothalamic action on cold-stimulated TSH secretion: an inhibition periventricularly, and a stimulation in the posterior hypothalamus.

Animals↗
PubMed1984

Immunoglobulin deposits in bladder epithelium and vessels in interstitial cystitis: possible relationship to circulating anti-intermediate filament autoantibodies.

Sera from patients suffering from interstitial cystitis (IC) reacted with bright staining of the bladder epithelium and vascular endothelium when tested for autoantibodies by indirect immunofluorescence using normal bladder tissue as target antigen. When tested for autoantibodies using cultured cells as antigen the antibodies were found to be directed against cytoskeletal intermediate filaments (IMF). Sera from 43 IC patients had a high incidence and high titers of anti-IMF autoantibodies as compared to both healthy individuals and patients suffering from other urological or surgical diseases. The results suggest that anti-IMF autoantibodies may be involved in the perpetuating chronic type of tissue injury seen in these patients. The antibodies were of the IgM class. In vivo deposits of IgM in patient bladder biopsies localized similarly to the autoantibodies; epithelial tissue showed deposits in 19% and vascular tissue, deposits in more than 50% of the patients, often together with complement components Clq,C3, or C4. In addition, subendothelial deposits associated with fibrillar structures could be observed. The results suggest a possible relationship between the in vivo IgM deposits in the bladder epithelium and vascular endothelium, on one hand, and the presence of anti-IMF antibodies capable of reacting with these cell structures, on the other hand. However, as the autoantibodies have to gain access to intracellular structures in order to cause in vivo deposits, primary tissue injury has to be postulated.

Adult↗
PubMed1984

Single- and multiple-dose pharmacokinetics of pipemidic acid in normal human volunteers.

The pharmacokinetic profile of pipemidic acid was studied in two groups of young healthy volunteers by using a new, sensitive, high-pressure liquid chromatography procedure for quantitation of pipemidic acid in biological fluids. After oral or intravenous administration, the disposition of pipemidic acid may be described as a one- or a two-compartment open model, respectively. Oral bioavailability was 93.1 +/- 11% (mean +/- standard error). After administration of a 100-mg tablet, 13.4 +/- 2.7% was bound to serum proteins at the time of peak drug concentration in serum. Excretion of pipemidic acid in saliva was negligible, the saliva/serum ratio being about 0.32. At steady state after the twice-daily administration of a 500-mg tablet, which is a recommended dosage regimen, a peak drug concentration in serum of 4.3 +/- 0.5 micrograms/ml was attained in 1.2 +/- 0.1 h. The apparent volume of distribution was 1.9 +/- 0.2 liters/kg, and the elimination half-life was 3.4 +/- 0.2 h. The renal clearance was 4.3 +/- 0.7 ml/min per kg, and the total clearance was 6.3 +/- 0.5 ml/min per kg. Despite a considerable water load, the minimum concentration in urine at the end of a dosing interval averaged 100 micrograms/ml, which widely exceeds the known MIC of pipemidic acid against bacteria commonly causing urinary tract infections.

Adult↗
PubMed1984

Bronchiolitis in rheumatoid arthritis.

Bronchiolitis in association with rheumatoid arthritis has been reported, to our knowledge, in 18 patients to date. In some cases use of penicillamine has been strongly associated with the development of bronchiolitis. Most of the reported cases are described as having marked irreversible airways obstruction and hyperinflation. We describe a patient with rheumatoid arthritis whose respiratory tract symptoms began during gold therapy. Physiologic studies showed marked lung hyperinflation without pathologic findings in forced dry spirometric study. On open lung biopsy a mild degree of granulomatous bronchiolitis was found. Immunofluorescent microscopy showed IgM- and IgG-containing plasma cells in the bronchiolar walls.

Adult↗
PubMed1984

Pharmacokinetics of graded oral doses of sulindac in man.

Pharmacokinetics of graded doses of sulindac were studied on 9 healthy volunteers. Serum concentrations of sulindac (inactive prodrug), sulindac sulfide (active metabolite) and sulindac sulfone (inactive metabolite) were measured both after a single dose of 150 mg, 175 mg or 200 mg and on the 6th and 7th days after b.i.d. administration of the same doses. The peak and minimum concentrations of sulindac were practically not dependent on the dose. The concentration-time curves remained similar after a single dose and after the repetitive dosing. On the contrary, both sulindac sulfide and sulfone gave about twice as high serum levels at steady-state as after a single dose. As judged from several pharmacokinetic parameters, a dose of 150 mg gave significantly smaller values than the higher doses but there was no significant difference between 175 mg and 200 mg in sulindac sulfide and sulfone concentrations. The average half-lives of sulindac, sulindac sulfide and sulfone were 1.7 -4.2 h, 15.3-16.1 h and 16.6-19.6 h, respectively. Both sulindac sulfide and sulfone tended to accumulate at a repetitive dose of 200 mg. The appropriate dose of sulindac appears to be 175 mg twice daily.

Adult↗
PubMed1983

Fine-structural evidence for vascular injury in patients with interstitial cystitis.

Bladder vessel walls of 20 patients with interstitial cystitis were studied by the electron microscope. 14 (70%) had severe endothelial injury. 10 (50%) showed injured smooth muscle cells. Odd basement membrane proliferations and disruptions were seen. Clusters of microfibrils about 10 nm in diameter and numerous partially membrane-bound vesicles of 100-600 nm with granular or tiny vesicular content ("granulovesicular bodies") were also seen. Intercellular junctions of endothelial cells were open and there was emigration of polymorphonuclear leucocytes and platelets. The findings show pronounced vascular injury to have taken place, with neoformation of elastic tissue. It is suggested that the injury is immunologically mediated and that particularly those clusters of connective tissue microfibrils not yet covered by an amorphous elastin component may be involved in the pathogenesis of this disease.

Biopsy↗