Localized morphea after breast implant for breast cancer: A case report.

PURPOSE: Early breast cancer follow-up guidelines for patients who underwent surgery suggest a regular and accurate clinical examination of the breast area, for an early identification of cutaneous or subcutaneous breast cancer relapse. Nonetheless, breast skin lesions arising in patients treated with mastectomy for breast cancer can be caused by several diseases. A series of diagnostic hypotheses should be considered, not only focusing on cutaneous metastasis, but also on dermatologic and systemic diseases. CASE REPORT: In February 2015, a 37-year-old patient underwent a right subcutaneous mastectomy for stage IIA breast cancer. Five months after beginning adjuvant chemotherapy, she noted hyperpigmentation and thickening of the skin on the right breast. Differential diagnosis included local relapse, skin infection, lymphoma, or primary cutaneous disease, and a skin biopsy was performed. The histopathologic specimen showed full-thickness sclerosis, with features of localized morphea. Therapy with clobetasol was prescribed, with progressive resolution of the thickness. The collaboration between many professionals in a multidisciplinary team (oncologist, dermatologist, plastic surgeon, and pathologist) was crucial to achieving the diagnosis. CONCLUSION: In the literature, some articles describe correlation between connective tissue diseases and silicone breast implants, but the pathogenetic mechanisms are unknown. We report a rare case of breast morphea after positioning a silicone implant in a patient who had undergone mastectomy. This clinical report represents an interesting model of multidisciplinary management of a patient with breast cancer who developed an uncommon dermatologic disease. Further studies are needed to clarify the association between silicone implants and breast morphea.

Development of an ecotoxicological protocol for the deep-sea fauna using the hydrothermal vent shrimp Rimicaris exoculata.

In light of deep-sea mining industry development, particularly interested in massive-sulphide deposits enriched in metals with high commercial value, efforts are increasing to better understand potential environmental impacts to local fauna. The aim of this study was to assess the natural background levels of biomarkers in the hydrothermal vent shrimp Rimicaris exoculata and their responses to copper exposure at in situ pressure (30MPa) as well as the effects of depressurization and pressurization of the high-pressure aquarium IPOCAMP. R. exoculata were collected from the chimney walls of the hydrothermal vent site TAG (Mid Atlantic Ridge) at 3630m depth during the BICOSE cruise in 2014. Tissue metal accumulation was quantified in different tissues (gills, hepatopancreas and muscle) and a battery of biomarkers was measured: metal exposure (metallothioneins), oxidative stress (catalase, superoxide dismutase, glutathione-S-transferase and glutathione peroxidase) and oxidative damage (lipid peroxidation). Data show a higher concentration of Cu in the hepatopancreas and a slight increase in the gills after incubations (for both exposed groups). Significant induction of metallothioneins was observed in the gills of shrimps exposed to 4µM of Cu compared to the control group. Moreover, activities of enzymes were detected for the in situ group, showing a background protection against metal toxicity. Results suggest that the proposed method, including a physiologically critical step of pressurizing and depressurizing the test chamber to enable the seawater exchange during exposure to contaminants, is not affecting metal accumulation and biomarkers response and may prove a useful method to assess toxicity of contaminants in deep-sea species.

Enhanced blood pressure response to cyclooxygenase inhibition in salt-sensitive human essential hypertension.

To evaluate the influence of salt sensitivity on the blood pressure response to oral indomethacin treatment, we studied 35 hospitalized essential hypertensive patients (24 men and 11 women, aged from 40 to 55 years). During a normal NaCl intake (120 mmol Na+ per day), patients were assigned to receive in a randomized double-blind fashion either 200 mg indomethacin (25 patients) or placebo (10 patients) for 5 days. Two weeks after the interruption of indomethacin treatment, during which the normal NaCl intake was continued, salt sensitivity was assessed by giving each patient a high (220 mmol Na+ per day for 10 days) and then a low (20 mmol Na+ per day for 10 days) NaCl diet. Blood pressure changes were evaluated, and the measurement taken at the end of the 2 weeks under normal sodium intake was considered baseline blood pressure. Patients were classified as salt sensitive when a diastolic blood pressure change of 10 mm Hg or more occurred after both low and high periods of sodium intake. In salt-resistant patients treated with indomethacin (n = 12, nine men and three women, mean age 50.5 +/- 3.7 years), neither blood pressure (systolic blood pressure from 150.8 +/- 11.2 to 154.6 +/- 9.3 mm Hg, NS; diastolic blood pressure from 99.3 +/- 2.1 to 101.1 +/- 4.4 mm Hg, NS) nor the urinary Na+ excretion (from 108.1 +/- 20.9 to 97.9 +/- 9.1 mmol/24 hr, NS) was significantly affected by the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Octreotide, a somatostatin analog, reduces insulin secretion and increases renal Na+ excretion in lean essential hypertensive patients.

The influence of insulin on renal Na+ excretion is still subject to debate. In order to evaluate the effect of insulin suppression on Na+ excretion, 20 never-treated essential hypertensive men and 8 normotensive men were studied. All subjects had a body mass index < 27 kg/m2. Both the glucose and the lipid metabolisms were normal. After 2 weeks under normal NaCl intake (120 mEq NaCl daily), either octreotide, a somatostatin analog, or vehicle were infused in a forearm vein during acute volume expansion (0.30 mL/kg/min isotonic saline given intravenously over a period of 30 min). A double-blind randomized cross-over design was followed, and each subject was given both infusions at a 1 week interval. Blood and urine samples were taken at times--60, 0, 30, 60, 90, 120, 180, 240, and 300 min. Our data showed that octreotide significantly lowered insulin levels in both hypertensives (from 12.2 +/- 2.4 microU/mL at time 0 to undetectable values at time 30 and 60 min) and normotensives (from 11.5 +/- 2.8 microU/mL at time 0, to undetectable values at time 30 and 60 min). Compared to saline infusion alone, octreotide significantly increased Na+ excretion in both hypertensives and normotensives (saline + octreotide v saline alone = P < .05 at time 60 and 90 min). In conclusion, octreotide enhanced the natriuretic response to intravenous Na+ load in both hypertensives and normotensives. The increase in urinary Na+ was accompanied by a significant decrease in plasma insulin levels.

Methods for detecting lupus anticoagulants and their relation to thrombosis and miscarriage in patients with systemic lupus erythematosus.

AIMS: To examine the sensitivity and specificity to past thrombotic events of four different coagulation tests, which screen for lupus anticoagulant (LA), and of anticardiolipin antibodies in patients with systemic lupus erythematosus. METHODS: Fifty three consecutive patients with systemic lupus erythematosus were studied of whom three males and 21 females, aged 21-60 years, had a history of venous and arterial thrombosis, or miscarriage, or both. Activated partial thromboplastin time (aPTT), dilute Russell's viper venom time (dRVVT), kaolin clotting time (KCT), dilute aPTT and the circulating titre of anticardiolipin antibodies were investigated in the two groups of patients and in 20 healthy control subjects. RESULTS: The prolonged dilute aPTT was more sensitive to thromboses or miscarriages, or both than dRVVT (p less than 0.05), KCT (p less than 0.01), and aPTT (p less than 0.001). No significant differences in specificity were found among aPTT (100%), dRVVT (93%), KCT (93%) and dilute aPTT (86.2%); but aPTT and dRVVT were significantly more specific (p less than 0.01, p less than 0.05, respectively) than anticardiolipin antibodies. CONCLUSIONS: The study shows a strong association between lupus anticoagulant and thrombosis when a very sensitive test such as the dilute aPTT is used. The combination of this assay with a very specific test such as dRVVT might enable patients with SLE at high risk of thrombosis to be identified.

Detection of replicative intermediates of viral RNA in peripheral blood mononuclear cells from chronic hepatitis C virus carriers.

Clinical and experimental evidence suggests the possible existence of one or more extrahepatic sites of HCV infection. In order to demonstrate the "in vivo" infection of lymphoid cells by HCV, we applied a nested PCR to total cytoplasmic RNA extracted from fresh or cultured peripheral blood mononuclear cells (PBMCs) of HCV chronically infected patients, using primers derived from the highly conserved 5' untranslated region of the HCV genome. The presence of virions in PBMCs occurs frequently, if not always, and is often accompanied by active viral replication. Moreover, the appearance of replicative intermediates after stimulation of cellular growth with mitogens suggests that latent genomes could undergo replication upon cellular activation and/or proliferation.

Geographical clustering of scleroderma in a rural area in the province of Rome.

A geographical cluster of scleroderma and scleroderma-related features was identified in a rural area in the province of Rome. Two patients with scleroderma, three with CREST syndrome and one with eosinophilic fasciitis were living in a village where the total population included 572 persons of voting age. No kindred relationships were demonstrable among these patients. Clinical features of scleroderma such as Raynaud's phenomenon, bilateral hand edema, and digital scars were detected in an additional 10 cases. A group of apparently healthy subjects with scleroderma-related serological abnormalities (circulating antinuclear and anticentriole autoantibodies) was also identified in the village. No disease-associated HLA antigen in the patients nor genetic differences between patients and healthy subjects living in the same village were detected by HLA typing. Some still unidentified environmental factors acting on genetically predisposed subjects may be responsible for the clustering of the disease seen in this study.

Microbial diversity in smoked salmon examined by a culture-independent molecular approach--a preliminary study.

Microbial biodiversity in sliced vacuum-packed cold smoked salmon was investigated using culture-independent molecular biology techniques. Sliced smoked salmon was stored for 25 days after being packed at 4 degrees C. DNA was extracted from sliced vacuum-packed cold smoked salmon. PCR DNA amplification were carried out using universal eubacterial primers corresponding to Escherichia coli 16S rRNA gene. 16S rRNA genes were amplified, cloned in E. coli and compared using Amplification Ribosomal DNA Restriction Analysis (ARDRA). 106 clones were studied and classified into 13 Operational Taxonomic Units (OTUs). Sequences obtained to describe those 13 OTUs were compared to GenBank data. They indicated the presence of Vibrio species. Enterobacteraceae and also marine psychrophilic clones related to Alteromonas macleodii, which were not encountered within cultures, but no Gram-positive species have been obtained. Those results indicate that bias in description of microbial diversity may be encountred in both molecular and cultural techniques.

Early effects of diabetes on inducible nitric oxide synthase in the kidney.

NO may be responsible for the glomerular hyperfiltration observed in diabetic kidney by inducing vasodilation of the afferent arteriole. The aim of this study was to evaluate which isoform of nitric oxide synthase (NOS) is responsible for increased renal production of NO in diabetic kidney. Thirty male WKY rats were divided into 6 groups. Five rats were sacrificed immediately, five after 20 days. In the other rats, diabetes was induced by streptozotocin. The four diabetic groups were sacrificed respectively after 5, 10, 15 and 20 days. Urine excretion of NO metabolites was assayed; immunochemistry showed the presence of inducible (iNOS) and endothelial constitutive (ecNOS) synthases in the kidney. Urinary excretion of NO metabolites increased significantly in diabetic rats five days after the induction of diabetes and at the end of the study whereas it was unchanged in the control group. Renal ecNOS remained unchanged throughout the study in all rats whereas iNOS increased significantly in diabetic rats from the fifth day until the end of the study. The results demonstrate that iNOS is activated in the kidney of rats, soon after the induction of diabetes, thus suggesting its involvement in the increased production of NO observed immediately after the onset of diabetes.

Reaction of dipyridamole with the hydroxyl radical.

Dipyridamole [2,6-bis-diethanolamino-4,8-dipiperidinopyrimido-(5,4-d)pyri midine], a well known platelet aggregation inhibitor, shows powerful hydroxyl radical scavenging activity by inhibiting OH.-dependent salicylate and deoxyribose degradation. Steady-state competition kinetics experiments with deoxyribose were carried out to evaluate the second-order rate constant for the reaction between hydroxyl radical and dipyridamole. OH. radicals were generated either by a Fenton-type reaction or by X-ray irradiation of water solutions. A second-order rate constant k(Dipyridamole + OH.) of 1.72 +/- 0.11 X 10(10) M-1 s-1 and of 1.54 +/- 0.15 X 10(10) M-1 s-1 was measured by Fenton chemistry and by radiation chemistry, respectively. Mannitol was used as an internal standard for hydroxyl radicals in steady-state competition experiments with deoxyribose. A rate constant K(Mannitol + OH.) of 1.58 +/- 0.13 X 10(9) M-1 s-1 and 1.88 +/- 0.14 X 10(9) M-1 s-1 was measured in the Fenton model and in the water radiolysis system, respectively. Both these rate constants are in good agreement with the published data obtained by the "deoxyribose assay" and by pulse radiolysis.

HBeAg/anti-HBe system and development of primary hepatocellular carcinoma in patients with HBsAg-positive liver cirrhosis.

The significance of the HBeAg/anti-HBe system and other HBV markers in the evolution of HBsAg-positive liver cirrhosis to primary hepato-cellular carcinoma (PHC) was studied by following up 70 cirrhotic patients from February 1978 to February 1981. Eight out of 19 (42.1%) patients with HBsAg positive liver cirrhosis developed PHC. On the other hand, only 7.8% of the patients with HBsAg-negative liver cirrhosis developed PHC. In the HBsAg-positive group only the patients who had already seroconverted to anti-HBe (7 out of 11) or were negative for both HBeAg and anti-HBe (1 out of 3) at the time of first observation and showed a histological picture of inactive cirrhosis, developed PHC during the follow-up period. No HBeAg-positive cirrhosis showed such an evolution. The absence of HBeAg in the sera of patients who developed PHC suggests that active HBV replication becomes increasingly defective during the course of malignant transformation.

Normalization of depressed natural killer activity after interferon-alpha therapy is associated with a low frequency of relapse in patients with chronic hepatitis C.

In the present study, we found that human recombinant interferon-alpha (rIFN-alpha) given at a dose of 3 x 10(6) units thrice weekly for three months, and 1.5 x 10(6) units thrice weekly for the next three months, was able to restore depressed natural-killer (NK) activity to normal values in 12 out of 21 chronic hepatitis C patients positive for anti-HCV antibodies. In all of these patients, NK normalization was still sustained after three months from suspension of therapy. Eighteen patients also showed a normalization of the alanine aminotransferase (ALT) level by the end of treatment (responder patients), independently of changes in NK activity. No significant improvement in either NK activity or aminotransferase levels was seen among 20 untreated patients. In 8 responder patients (1 with normalized and 7 with low NK activity), ALT levels returned to pre-therapy values within three months after suspension of rIFN-alpha administration (relapse). We found that patients who normalized NK activity had a lower frequency of relapse as compared to patients with low NK activity by the end of treatment (p > 0.01). Immunofluorescence analysis of biopsy-derived liver tissue revealed that rIFN-alpha was able to induce strong MHC class I antigen expression on hepatocytes of treated patients, but this was not related to the clinical course.

Immunology of hepatocellular carcinoma.

The immune surveillance theory continues to remain a powerful force in cancer research and therapy despite the varying degrees of enthusiasm from both its supporters and critics. The role of both specific and non-specific immune responses in the host's defense against hepatocellular carcinoma is presented as well as the possibilities of immune-system manipulation for the prevention and therapy of this tumour.

Involvement of Phospholipase A(2) in H(2)O(2)-dependent Platelet Activation.

Hydrogen peroxide (H(2)O(2)) triggers activation of platelets 'primed' by low concentrations of arachidonic acid (< 20 µM) or collagen (< 0.2 µg/ml), but has no effect on platelets exposed to low concentrations of thrombin, ADP or A23187. Platelets are not affected (they do not aggregate or produce thromboxane A(2) or release serotonin) by H(2)O(2) alone or by the low concentrations of arachidonic acid or collagen. The H(2)O(2) concentration used (0.15-7.5 µM) induces aggregation, TA(2) production and dense granule content release (monitored by radiolabeled serotonin) by 'primed' platelets. Using arachidonic acid as the 'priming' stimulus, K(app) of 687 nM and 560 nM are calculated for platelet aggregation and TA(2) formation respectively. With collagen as the 'priming' stimulus, K(app) of 841 nM and 946 nM are obtained for platelet aggregation and TA(2) production, respectively. The effect of H(2)O(2) is dependent on arachidonic acid metabolism because aspirin prevents H(2)O(2)-mediated platelet activation. Furthermore this activation seems to be dependent on arachidonic acid mobilization from platelet phospholipids by phospholipase A(2) since mepacrine is able to block H(2)O(2)-mediated platelet activation.