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Biomedical subjects

A Luini

Publications and source records attributed to A Luini.

At least 127 records · Page 7Linked to original sources
PubMed1989

Percutaneous transthoracic needle aspiration biopsy: a case report of implantation metastasis.

Dissemination of tumor cells along the needle tract after needle aspiration biopsy has been reported in the literature, but it is an extremely uncommon event, especially when 'fine needles' (above 21 Gauge) are used. In the work presented, a patient with a mammary nodule of doubtful nature is reported. After histological evaluation the node proved to be an intra-mammary dissemination of poorly differentiated adenocarcinoma of the lung via the needle track after aspiration biopsy. The needle used was a 20 Gauge, which is not included in the fine needle category recommended by most authors. The possibility of tumor cells dissemination after needle biopsies is discussed.

Adenocarcinoma↗
PubMed1988

Dual regulation of ACTH secretion by guanine nucleotides in permeabilized AtT-20 cells.

1. We have examined the effects of guanine nucleotides on ACTH secretion from digitonin-permeabilized AtT-20 cells, with the aim of analyzing the involvement of GTP-binding proteins (G proteins) in the secretory process. 2. AtT-20 cells permeabilized with 20 microM digitonin displayed calcium-dependent secretion. The EC50 of calcium was approximately 2 microM and the maximal stimulation was 350% of basal release. 3. Nonhydrolyzable guanine nucleotides also stimulated ACTH release, in a virtually Ca2+-free medium. The EC50 of guanosine 5'-(3-O-thio)triphosphate (GTP gamma S) was approximately 15 microM and the maximal stimulation was approximately 230% of basal release. The effects of calcium and guanine nucleotides were not additive. 4. In the presence of the inhibitory hormone, somatostatin guanine nucleotides inhibited the calcium-stimulated secretion. 5. Both the stimulatory and the inhibitory effects on secretion of guanine nucleotides were independent of changes in cyclic AMP (cAMP) and calcium. It is suggested that G proteins influence an unknown step in the secretion process, which would be near or at the exocytotic site. 6. The results can be explained by assuming the existence of two types of G proteins, one with stimulatory effects on exocytotic release (GeS) and another with inhibitory effects (GeI).

Adrenocorticotropic Hormone↗
PubMed1988

Resectable breast cancer: axillary dissection sparing pectoralis muscles and nerves.

In breast cancer surgery, axillary dissection is currently considered an essential step. Nevertheless, procedures commonly used include the resection of the pectoralis minor muscle and/or pectoralis nerves. Since 1984 we have performed axillary dissection by sparing both the pectoralis muscles and their nerves. In this paper we present the surgical technique. The comparison of the two groups with clinical N0 N1a assessment, the former of 103 patients submitted to this kind of surgical procedure, the latter (108 women) treated by resection of the pectoralis minor muscle, showed that the mean number of dissected lymph nodes in both procedures was superimposable.

Axilla↗
PubMed1987

Young age is not an ominous prognostic factor in breast cancer patients.

Analysis of a series of 137 women 20-30 years of age, operated for breast carcinoma, excluding patients pregnant, lactating or with inflammatory cancer, showed that disease-free survival rates were similar and not lower than those reported for a large series of 716 breast cancer patients of all ages, treated and followed at the same Institute. Ten-year disease-free survival rates for the two series of 137 young women and 716 patients of all ages were 43.7% and 47.1% respectively. Even when considering the subgroups of patients with and without nodal axillary involvement, the corresponding figures for the two series considered were 72.6% vs. 72.1% (N-) and 25.1% vs. 24.5% (N+). It can be concluded that young age cannot be considered as an unfavorable prognostic factor.

Adult↗
PubMed1987

Distribution of axillary node metastases by level of invasion. An analysis of 539 cases.

Five hundred and thirty-nine patients with carcinoma of the breast treated with total axillary dissection and with positive axillary nodes were evaluated. The total number of lymph nodes removed was 11,082, with an average of 20.5 nodes per patient. The average number of lymph nodes at the first level was 13.8, at the second level 4.5, at the third level 2.2. The average number of nodes was 20.7 in cases treated with Halsted mastectomy, 20.9 with total mastectomy and axillary dissection, 20.3 with quadrantectomy and axillary dissection. Of 3259 metastatic nodes, 64 were site of micrometastases; 797 were partially involved, 441 were totally involved and 1957 were site of metastases with extracapsular invasion. In 314 (58.2%) the first level only was involved, in 117 cases (21.7%) metastases were present at the first and second level, whereas in 88 cases (16.3%) all the three levels were sites of metastases. Only 20 cases showed skipping distribution. In 1.5% of the cases the first level was skipped by metastases, in 0.4% the first nodes of the first level are clear the chances that metastatic nodes are present at the second and third levels are negligible. When the nodes at the first level are positive, the chances that metastases are also present at the higher levels are of the order of 40.0%.

Axilla↗
PubMed1987

Preliminary clinical studies with PDT by topical TPPS administration in neoplastic skin lesions.

Cutaneous photosensitization by topical administration of a porphyrin derivative has been previously reported from experimental studies. Preliminary clinical trials performed at the National Cancer Institute of Milan in the last six months have confirmed the feasibility of treating skin lesions by topical application of photosensitizers. Fourteen cases of basal cell carcinoma were treated by local administration of tetraphenylporphinesulphonate (TPPS), vehicled by azone. Later, the tumor was exposed to a wavelength of 630 nm from a dye laser. We noted complete remission, as documented by biopsies, in all tumors, with clinical thickness less than 2 mm, whereas partial remission was obtained in tumors with clinical thickness more than 2 mm. Our experience suggests the possibility of a routine treatment by this method for flat basal cell carcinoma and pre-malignant lesions, with remarkable advantages to conventional therapies. Our results have to be confirmed by increasing the number of cases and length of follow up; our short follow up does not allow us to make definitive claims regarding this therapy.

Administration, Topical↗
PubMed1987

Norepinephrine and thyrotropin stimulation of iodide efflux in FRTL-5 thyroid cells involves metabolites of arachidonic acid and is associated with the iodination of thyroglobulin.

Ca2+-dependent and TSH-, norepinephrine (NE)-, and A23187-induced iodide (I-) efflux from FRTL-5 rat thyroid cells is inhibited by quinacrine and trifluoroperazine, agents that inhibit phospholipase A2 activity. Furthermore, I- efflux can be stimulated by an activator of phospholipase A2 activity, melittin. Phospholipase A2 action releases arachidonic acid from phospholipids; arachidonic acid enhances I- efflux in FRTL-5 cells. Inhibitors of arachidonic acid metabolism via the lipoxygenase pathway, 5,8,11,14-eicosatetraynoic acid and nordihydroguaiaretic acid, and via the cytochrome P450-linked epoxygenase pathway, piperonyl butoxide and 2-diethylaminoethyl-2,2-diphenyl valerate, but not an inhibitor of the cyclooxygenase pathway, indomethacin, can inhibit TSH-, NE-, and A23187-induced I- efflux. TSH, NE, and arachidonic acid stimulation of I- efflux in FRTL-5 cells is associated with increased iodination of thyroglobulin, which is blocked by 10 microM 5,8,11,14-eicosatetraynoic acid and 50 microM piperonyl butoxide. The data thus suggest that TSH- and NE-induced I- efflux from FRTL-5 thyroid cells involves lipoxygenase and/or epoxygenase metabolites of arachidonic acid, released from phospholipids upon Ca2+-dependent activation of phospholipase A2. Since this process is associated with the iodination of thyroglobulin, TSH- and NE-induced I- efflux in FRTL-5 cells may represent the transport of I- from the cell into the follicular lumen in vivo.

Animals↗
PubMed1987

Contralateral breast cancer after limited surgery plus radiotherapy of early mammary tumors.

Conservative treatment of early breast cancer with limited surgery requires a mandatory irradiation of the affected breast, which implies a low but measurable irradiation of contralateral breast too. As ionizing radiations can produce an oncogenic effect on mammary tissues, the series of 701 patients of the Milano clinical trial on T1 No breast cancer (1973-1980) was investigated to compare the incidence of contralateral breast cancer in the Halsted group (not irradiated) and in the QU.A.RT. group (irradiated on the operated breast with a total dose of 50 Gy plus a limited boost of 10 Gy). In March 1986, a contralateral breast cancer was diagnosed in 17/349 patients (4.9%) of the Halsted group and in 18/352 patients (5.1%) of the QU.A.RT. group after a median follow-up of 108 months. The sites of contralateral cancer were superimposable in the two groups of patients, with a constant prevalence of external quadrants, despite the great difference of dose distribution in the irradiated patients. Our data on the incidence of contralateral breast cancer failed to demonstrate an oncogenic effect of irradiation to date, but the follow-up is still in progress and any future event will be registered and discussed.

Axilla↗
PubMed1986

Alpha 1-adrenergic stimulation of arachidonic acid release and metabolism in a rat thyroid cell line. Mediation of cell replication by prostaglandin E2.

The rat thyroid cell line, FRTL-5, expresses an alpha 1-adrenergic receptor when exposed to thyrotropin. We have found that occupation of this alpha 1-adrenergic receptor by norepinephrine stimulated the release of [3H]arachidonic acid from prelabeled cells. Arachidonic acid was metabolized primarily to prostaglandin E2 and to much smaller amounts of 11-hydroxy-5,8,11,13-eicosatetraenoic acid, 15-hydroxy-5,8,11,13-eicosatetraenoic acid, prostaglandin D2, and thromboxane B2. Synthesis of all these metabolites was inhibited by the cyclooxygenase inhibitor indomethacin. When FRTL-5 cells were starved of thyrotropin for 24 h, norepinephrine nearly doubled [3H]thymidine uptake into DNA. Cyclooxygenase inhibitors inhibited norepinephrine-stimulated thymidine uptake by 60-70%. Of several arachidonic acid metabolites tested, none was able to stimulate thymidine uptake directly in the presence of indomethacin. Prostaglandin E2, however, was able to restore [3H]thymidine uptake when added together with norepinephrine in the presence of indomethacin. Thus, occupation of an alpha 1-adrenergic receptor in a functional rat thyroid cell line leads to arachidonic acid release. Subsequent metabolism of the arachidonic acid by the cyclooxygenase pathway leads to synthesis of prostaglandin E2, which mediates a norepinephrine-stimulated activity related to cell replication.

Adrenergic alpha-Agonists↗
PubMed1986

Comparison of Halsted mastectomy with quadrantectomy, axillary dissection, and radiotherapy in early breast cancer: long-term results.

From 1973 to 1980 we randomly assigned 701 patients with breast cancer measuring less than 2 cm in diameter and with no palpable axillary lymph nodes to Halsted radical mastectomy (n 349) or to 'quadrantectomy' with axillary dissection and radiotherapy to the ipsilateral breast tissue (n 352). The two groups were comparable in age distribution, size and site of primary tumor, menopausal status, and frequency of axillary metastases. The average follow-up time was 103 months. Actuarial curves show no difference between the two groups in the disease-free interval after surgery or in the overall survival rate. At 8 yr the disease-free survival was 77% for the patients in the Halsted group and 80% for those in the 'quadrantectomy' group, and the overall survival was 83 and 85% respectively. We conclude that small breast cancers may be safely treated with the conservative treatment described. In our opinion total ablative operations are not justified.

Axilla↗
PubMed1986

Local control and survival in early breast cancer: the Milan trial.

From 1973 to 1980, 701 patients with breast cancer measuring less than 2 cm in pathological diameter and with no palpable axillary lymph nodes were randomized to Halsted mastectomy (349) or to "quadrantectomy" with axillary dissection and radiotherapy to the ipsilateral breast tissue (QUART) (352). The two groups were comparable in age distribution, size and site of primary tumor; menopausal status; and frequency of axillary metastases. At 8 years, the disease-free survival was 77% for the Halsted patients and 80% for the "quadrantectomy" patients, while overall survival was 83% and 85%, respectively. Disease-free and overall survival curves show no difference between the two groups. Breast cancer of small size (less than 2 cm) may be safely treated with conservative treatment. Mutilating operations are not justified.

Aged↗
PubMed1986

Phospholipase A2 and phospholipase C are activated by distinct GTP-binding proteins in response to alpha 1-adrenergic stimulation in FRTL5 thyroid cells.

In FRTL5 rat thyroid cells, norepinephrine, by interacting with alpha 1-adrenergic receptors, stimulates inositol phosphate formation, through activation of phospholipase C, and arachidonic acid release. Recent studies have shown that GTP-binding proteins couple several types of receptors to phospholipase C activation. The present study was undertaken to determine whether GTP-binding proteins couple alpha 1-adrenergic receptors to stimulation of phospholipase C activity and arachidonic acid release. When introduced into permeabilized FRTL5 cells, guanosine 5'-[gamma-thio]triphosphate (GTP[gamma-S]), which activates many GTP-binding proteins, stimulated inositol phosphate formation and arachidonic acid release. Neomycin inhibited GTP[gamma-S]-stimulated inositol phosphate formation but was without effect on GTP[gamma-S]-stimulated arachidonic acid release, suggesting that separate GTP-binding proteins mediate each process. In addition, pertussis toxin inhibited norepinephrine-stimulated arachidonic acid release but not norepinephrine-stimulated inositol phosphate formation. Norepinephrine-stimulated arachidonic acid release but not inositol phosphate formation was also inhibited by decreased extracellular calcium and by TMB-8, suggesting a role for a phospholipase A2. To confirm that arachidonic acid was released by a phospholipase A2, FRTL5 membranes were incubated with 1-acyl-2-[3H]arachidonoyl-sn-glycero-3-phosphocholine. GTP[gamma-S] slightly stimulated arachidonic acid release, whereas norepinephrine acted synergistically with GTP[gamma-S] to stimulate arachidonic acid release. The results show that phospholipase C and phospholipase A2 are activated by alpha 1-adrenergic agonists. Both phospholipases are coupled to the receptor by GTP-binding proteins. That coupled to phospholipase A2 is pertussis toxin-sensitive, whereas that coupled to phospholipase C is pertussis toxin-insensitive.

Animals↗
PubMed1986

A guanine nucleotide-binding protein mediates the inhibition of voltage-dependent calcium current by somatostatin in a pituitary cell line.

Somatostatin reduces voltage-dependent Ca2+ current (ICa) and intracellular free Ca2+ concentration in the AtT-20/D16-16 pituitary cell line. We tested whether guanine nucleotide-binding proteins (G or N proteins) are involved in the signal transduction mechanism between the somatostatin receptor and voltage-dependent Ca2+ channels. Treatment of the cells with pertussis toxin, which selectively ADP ribosylates the GTP binding proteins Gi and Go and suppresses the ability of Gi to couple inhibitory receptors to adenylate cyclase, abolished the action of somatostatin on both ICa and intracellular free Ca2+. Intracellular application of the nonhydrolyzable guanine nucleotide analog guanosine 5'-[gamma-thio]triphosphate (GTP[gamma S]), which irreversibly activates G proteins, changed the somatostatin effect on ICa from a reversible to an irreversible inhibition. Intracellular GTP[gamma S] alone caused a very slowly developing inhibition of ICa. When ICa was inhibited by GTP[gamma S] (alone or with somatostatin), it failed to respond to subsequent applications of somatostatin. The effect of GTP[gamma S] on the inhibition of ICa by somatostatin was not altered by the intracellular application of cAMP and 3-isobutyl-1-methylxanthine. The results suggest that a GTP-binding protein is directly involved in the cAMP-independent receptor-mediated inhibition of voltage-dependent Ca2+ channels.

Adenylate Cyclase Toxin↗
PubMed1986

Forskolin enhances basal and potassium-evoked hormone release from normal and malignant pituitary tissue: the role of calcium.

The release of immunoreactive ACTH (IR-ACTH) from AtT-20 pituitary tumor cells was transiently increased by exposure to an elevated concentration of potassium ion in an osmotically balanced extracellular medium. With the calcium-sensitive dye Quin 2, the concentration of free cytosolic calcium (Cai) in the AtT-20 tumor was determined to be 115 nM. Challenge of these cells with 60 mM potassium in an osmotically balanced salt solution raised the concentration of Cai to 246 nM. This is in accord with the view that agents promoting calcium entry into pituitary cells trigger hormone secretion. Addition of forskolin to the extracellular medium caused a sustained release of IR-ACTH from AtT-20 tumor cells. Challenge with forskolin (10 microM) increased the concentration of Cai to 149 nM. This observation is also in accord with the view that calcium entry is a necessary and sufficient stimulus to trigger hormone secretion from the anterior pituitary lobe. Exposure of cells to forskolin (10 microM) before a potassium challenge increased the quantity of IR-ACTH released in response to potassium, but did not alter the minute by minute time course of the response to this ion. Forskolin pretreatment did not alter the potassium-evoked rise in Cai concentration. This observation suggests that the magnitude of the secretory response of the pituitary gland can be enhanced by agents other than those promoting an increase in Cai. After exposure of the tumor cells to potassium for a sufficient time to permit the rate of release of hormone to return to the basal value, forskolin could still stimulate the release of hormone from the tumor cells. Under these circumstances, forskolin did not increase the concentration of Cai. This observation suggests that pituitary hormone secretion can be initiated by a factor(s) other than an acute change in the Cai concentration. Both forskolin and 8-bromo-cAMP stimulated hormone secretion from dispersed melanotrophs and potentiated the potassium-evoked secretory response of these cells. Neither compound affected the apparent time course of the response to potassium. These observations suggest that the effects of forskolin and potassium on the AtT-20 tumor cell may use mechanisms occurring in normal pituitary cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1986

Somatostatin, an inhibitor of ACTH secretion, decreases cytosolic free calcium and voltage-dependent calcium current in a pituitary cell line.

Somatostatin is a neurohormone peptide that inhibits a variety of secretory responses in different cell types. We have investigated the effects of somatostatin on calcium current and intracellular free calcium in AtT-20 cells, a pituitary tumor line in which the inhibitory actions of this peptide have been well characterized. At concentrations similar to those that inhibit adrenocorticotropic hormone (ACTH) release, somatostatin and its analogs reduced the levels of intracellular free calcium (as measured by the Quin-2 technique). Nifedipine and other blockers of voltage-dependent calcium channels also reduced cytosolic calcium levels. The effects of somatostatin and nifedipine were not additive, suggesting that somatostatin might inhibit calcium channels. Experiments using the whole-cell patch-clamp technique showed that somatostatin reduces voltage-dependent calcium current. The effects of somatostatin on cytosolic calcium and calcium current appear to be independent of its ability to reduce secretagogue-stimulated cAMP accumulation in these cells. We propose that the somatostatin-induced decrease in cytosolic calcium concentrations and the voltage-dependent calcium current are one of the mechanisms by which somatostatin suppresses ACTH release in AtT-20 cells.

Adrenocorticotropic Hormone↗
PubMed1985

Association of the changes in cytosolic Ca2+ and iodide efflux induced by thyrotropin and by the stimulation of alpha 1-adrenergic receptors in cultured rat thyroid cells.

Thyrotropin causes a time- and concentration-dependent increase in cytosolic Ca2+ in FRTL-5 rat thyroid cells as measured by Quin2 fluorescence; the half-maximal response occurs in response to 1 X 10(-7) M thyrotropin. The effect of added thyrotropin is the same whether cells have been previously and chronically exposed to thyrotropin or whether they have been thyrotropin "starved" for several days. The thyrotropin effect on cytosolic Ca2+ has no relationship to intracellular cAMP levels with respect to dose and time course. Norepinephrine (1 X 10(-7) M) also causes increases in cytosolic Ca2+ in FRTL-5 thyroid cells. With the use of a variety of adrenergic inhibitors, norepinephrine was found to exert its effect via an alpha 1-adrenergic receptor. The exposure of FRTL-5 cells to physiological thyrotropin concentrations enhances the effect on cytosolic Ca2+ level induced by norepinephrine in vitro; the shape of the dose-response curve indicates a cooperative effect of the thyrotropin and norepinephrine. The increase in cytosolic Ca2+ seems to be derived from an intracellular pool rather than from the extracellular space. It is not prevented by nifedipine, a blocker of Ca2+ channels; it is present in cells exposed to ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid; and it is not associated with increased Ca2+ uptake into the cell. the thyrotropin- and norepinephrine-induced increase in cytosolic Ca2+ parallels the efflux of iodide and the organification of thyroglobulin in a dose-dependent manner.

Adrenergic alpha-Antagonists↗