Stainless steel weld metal enhanced with carbon nanotubes.

This paper aims to establish the most indicated route to manufacture a nanostructured powder composed of 5 wt% Multi-walled Carbon Nanotubes and 304LSS powder. Four specimens were prepared using Mechanical Alloying and Chemical Treatment (CT) with Hydrogen Peroxide ([Formula: see text]) as the main processes. A thermal treatment post-processing was used in half of the samples to remove the remaining amorphous carbon and to evaluate its effects. Regarding the powder analysis, attachment, amorphous carbon degree, crystallinity, and doping of the CNT throughout the metal matrix were investigated. The nanostructured powders were then inserted as a core in a 304LSS tubular rod to perform the arc welding process. The CT route eliminated the amorphous carbon and generated more refiner grains, which provided a cross-section hardness gain of more than 40% regarding the 304LSS joint. In summary, the CT route, combined with the GTAW process, provided a new method for nanocomposite manufacturing by combining shorter preparation steps, obtaining an improvement in the microstructural and hardness performance.

In Situ Cytokine Expression and Morphometric Evaluation of Total Collagen and Collagens Type I and Type III in Keloid Scars.

Keloids are characterized by excessive collagen deposition and growth beyond the edges of the initial injury, and cytokines may be related to their formation. The objective of this study was to evaluate the collagen fibers, analyze in situ expression of cytokines in keloid lesions, and compare to the control group. Results showed that there was a predominance of women and nonwhite and direct black ancestry. Keloid showed a significant increase in total and type III collagen. Significantly, the expression of mRNA for TGF-ß in keloid was increased, the expressions of IFN-γ, IFN-γR1, and IL-10 were lower, and IFN-γR1 and TNF-α had no statistical difference. Correlations between collagen type III and TGF-ß mRNA expression were positive and significant, IFN-γ, IFN-γR1, and IL-10 were negative and significant, and TNF-α showed no statistical difference. We conclude that there was a significant increase of total collagen in keloid and predominance of collagen type III compared to the controls, showing keloid as an immature lesion. There is a significant increase in TGF-ß mRNA in keloid lesions, and a significant decrease in IFN-γ and IL-10, suggesting that these cytokines are related to keloid lesions.

Physical training induces expression of TGF-beta in kidney of pregnant hypertensive rats.

AIM: This study aimed to determine the morphological renal impairment in pregnant rats spontaneously hypertensive (SHR) submitted to swimming when compared with those who did not perform the activity, and to analyze the relationship of expression of cytokines in inflammatory fibrotic and protrained and sedentary animals. METHODS: SHRs and their respective control normotensive rats (WKY) were submitted or not to a swimming protocol during 9 weeks, resulting in four pregnant experimental groups: sedentary hypertensive (HS), trained hypertensive (HT), sedentary normotensive (NS), and trained normotensive (NT). RESULTS: Pregnant untrained hypertensive rats presented higher resting mean blood pressure (MAP) compared with both sedentary and trained normotensive groups (P<0.05). We can observe too, that the exercise training did not change the heart rate (HR) in both hypertensive and normotensive groups (P=0.127). The HT rats showed lower area of mesangial matrix (MM) compared to NT group (P=0.018). The perceptual of fibrosis (%F) in hypertensive rats was significantly higher compared with the % F in normotensive rats (P<0.001). The rats in the HT group showed higher expression of TGF-b (P<0.001) and of IL-10 (P<0.001) when compared with the other groups. CONCLUSION: The main conclusion is that in SHR rats it is shown a greater expression of TGF-beta, resulting in increased fibrosis in renal parenchyma due to the increased number of inflammatory cells that secrete this cytokine, and thus the practice of swimming can attenuate inflammatory processes, and mitigate the blood pressure of these animals.

NF-kB expression in IgA nephropathy outcome.

Some studies have demonstrated the involvement of nuclear factor-kappa B (NF-kB) in the pathogenesis of glomerulonephritis. The aim of our study was twofold: (1) to analyze the prognostic value of NF-kB expression in primary IgA nephropathy (IgAN) and (2) to compare the results of NF-kB expression by immunohistochemistry (IHC) and southwestern histochemistry (SWH). We analyzed 62 patients diagnosed with IgAN from 1987 to 2003. We used monoclonal antibodies to CD68 and mast cell tryptase and polyclonal antibodies to TGF-ß1, α-SMA and NF-kB p65. We used SWH for the in situ detection of activated NF-kB. The results showed that NF-kB expression (mainly by SWH) correlated with clinical and histological parameters. An unfavorable clinical course of IgAN was significantly related to tubular NF-kB expression by SWH, but not by IHC. The Kaplan-Meier curves demonstrated that increased NF-kB expression, which was measured by IHC and SWH, decreased renal survival. In conclusion, the increased expression of NF-kB in the tubular area may be a predictive factor for the poor prognosis of patients with IgAN. Compared with IHC, NF-kB expression determined by SWH was correlated with a larger number of parameters of poor disease outcome.

Mast cells, TGF-beta1 and alpha-SMA expression in IgA nephropathy.

IgA nephropathy (IgAN) is a kidney disease with a varying renal prognosis. Recently, many studies have demonstrated that renal alpha-smooth muscle actin (alpha-SMA) and transforming growth factor (TGF-beta1) expression, as well interstitial mast cell infiltrates could represent a prognostic marker in several renal diseases. The aim of our study was to analyze the prognostic value of mast cell, TGF-beta1 and alpha-SMA expression in IgAN. A survey of the medical records and renal biopsy reports of 62 patients with a diagnosis of IgAN followed-up from 1987 to 2003 was performed. The mean follow-up time was 74.7 +/- 50.0 months. The immunohistochemical studies were performed using a monoclonal antibody anti-human mast cell tryptase, a polyclonal antibody anti-human TGF-beta1, and a monoclonal antibody anti-human alpha-SMA. An unfavorable clinical course of IgAN was related to interstitial mast cell infiltrates and alpha-SMA expression in the tubulointerstitial area. Expression of glomerular TGF-beta1 and alpha-SMA, and interstitial TGF-beta1 is not correlated with clinical course in IgAN. In conclusion, the increased number of mast cells and higher alpha-SMA expression in the tubulointerstitial area may be predictive factors for the poor prognosis of patients with IgAN.

Quantitative analysis of fibrosis and mast cells in the tongue of chronic chagasic patients: autopsy study.

OBJECTIVE: Recently, an orally transmitted outbreak of Chagas disease was reported in Santa Catarina, Brazil, after ingestion of sugar cane juice (garapa). This disease is caused by Trypanosoma cruzi, a parasite that stimulates the development of chronic inflammatory response, characterized by fibrous connective tissue neoformation (fibrosis). As the density of tissue mast cells (MC) may be an index of fibroblast proliferation and development of local fibrosis, the purpose of this autopsy study was to quantify the fibrosis rate and the number of MC in the tongues of chronic chagasic (CC) patients, compared with a non-chagasic (NC) control group. METHODOLOGY: Twenty-four evaluations, with a quantitative assessment of fibrosis percentage and MC density were performed. RESULTS: The percentage of fibrosis in the tongue was higher among CC than in the control group. In the CC group, a positive and significant correlation was found when the fibrosis rate was compared with the MC density. CONCLUSIONS: These morphometric findings suggest that tongue biopsy may be useful to study specific changes associated with Chagas disease. They also suggest that the systematic analysis of oral cavity, including tongue histopathology changes, could be useful in forensic pathology of the orally acquired chronic Chagas disease.

A role for HO-1 in renal function impairment in animals subjected to ischemic and reperfusion injury and treated with immunosuppressive drugs.

INTRODUCTION: Ischemia/reperfusion injury (IRI) represents the single major antigen-independent factor implicated in pathogenesis of chronic graft dysfunction. Tacrolimus is a calcineurin inhibitor, which has been suggested to be helpful in cyclosporine-related chronic toxicity. Rapamycin has antiproliferative properties that may impair renal regeneration after IRI. Therefore, immunosuppressive drugs might impair renal graft outcome in those organs suffering IRI. MATERIAL AND METHODS: C57B1/6 male mice subjected to 45 minutes of renal pedicle ligation were reperfused for 24 hours. Mice were treated with rapamycin, cyclosporine, or tacrolimus. Blood and renal tissue samples were collected at 24 hours after IRI. Urea levels were measured. Heme Oxygenase 1 (HO-1) gene transcript was amplified by a real-time polymerase chain reaction technique. RESULTS: Animals treated with cyclosporine and subjected to IRI showed impaired renal function that peaked at 24 hours. Additional pretreatment with rapamycin produced even more impairment of renal function, when compared with controls. However, tacrolimus pretreatment was associated with a better renal outcome. HO-1 expression was upregulated after IRI by 2.6 arbitrary units at 24 hours. Rapamycin showed worse impairment of renal function. CONCLUSION: Tacrolimus was not associated with worsening renal function when compared with animals just subjected to IRI. Upregulation of HO-1 may be an attractive approach to limit graft injury.

The effects of rapamycin in the progression of renal fibrosis.

UNLABELLED: Renal fibrosis is a hallmark of end-stage renal diseases and of chronic allograft nephropathy (CAN). Rapamycin, besides its action through blockade of lymphocyte proliferation, also has antiproliferative, antiviral, and antitumor actions. Its use in clinical in patients with CAN has recently been advocated. OBJECTIVES: Our goal was to evaluate the effect of rapamycin in an established model of renal fibrosis, unilateral ureteral obstruction. MATERIALS AND METHODS: C57BL/6 mice were divided into two groups, treated or not with daily doses of rapamycin (0.2 mg/kg) beginning on day-1. The obstruction was performed as day 0. Blood and kidney tissues were collected at 1, 4, 7, and 14 days after the surgery to quantify bone morphogenic protein (BMP)-7 and transforming growth factor (TGF)-beta mRNA by real time PCR. RESULTS: Daily treatment with rapamycin caused a significant reduction in serum creatinine at day 1 (0.57 +/- 0.03 vs 0.95 +/- 0.15 mg/dL, P = .002) and at day 14 (0.56 +/- 0.04 vs 0.73 +/- 0.07 mg/dL, P = .040). This profile was corroborated by histological morphometric analyses showing less fibrosis at day 14. However, rapamycin surprisingly induced an upregulation of TGF-beta at day 4 (3.05 +/- 0.46 vs 1.85 +/- 0.41, P = .006) and at day 7 (6.33 +/- 0.55 vs 4.97 +/- 0.38, P = .024) with a reduced expression by day 14 (4.03 +/- 1.07 vs 7.89 +/- 0.83, P < .001). Surprisingly, rapamycin also promoted an increment in BMP-7, completely reversing the ratio of TGF-beta to BMP-7, allowing a more protective phenotype. CONCLUSION: Rapamycin slightly ameliorated the renal dysfunction and, at later time points, induced less fibrosis and less decrease in the TGF-beta to BMP-7 ratio.

Dual response of animals with chronic cyclosporine nephrotoxicity to an acute ischemic injury.

Normal kidneys regenerate after acute injury with little development of chronic fibrosis. However, the long-term effects of an acute injury in kidneys with established chronic toxicity induced by cyclosporine (CsA) are not entirely clear. To study the consequences of an ischemia and reperfusion (IR) injury in long-term CsA-treated rats, male Wistar rats (250-300 g) were treated daily with CsA (10 mg/kg) or vehicle (olive oil 1 mL/kg) for 28 days. On day 21, ischemia was performed by clamping the renal vessel for 1 hour. Blood samples were collected on days 0 and 21 (before IR) as well as days 22 and 28. On day 28, the kidneys were collected to examine the mRNA expression of MCP-1 by real-time PCR. For renal function, serum creatinine levels were measured. Twenty-four hours after reperfusion, long-term CsA-treated animals showed better renal function compared with the control group, as demonstrated by serum creatinine levels: 2.2 +/- 0.13 mg/dL vs 2.9 +/- 0.18 mg/dL, respectively (P < .05). However, 1 week after IR, the renal function was worse among the long-term CsA-treated group than the controls: 1.16 +/- 0.08 mg/dL vs 0.8 +/- 0.09 mg/dL, respectively (P < .05). Interestingly, CsA treatment was associated with lower MCP-1 mRNA expression than that in the control group: mean MCP-1 mRNA expression 0.58 +/- 0.13 vs 1.02 +/- 0.12, respectively (P < .05). In conclusion, animals with chronic CsA nephrotoxicity were protected from an acute renal injury, possibly through decreased chemokine production, although at later time points, renal function was clearly impaired, probably by the acceleration of vasculopathy caused by nephrotoxicity.

The role of heme oxygenase 1 in rapamycin-induced renal dysfunction after ischemia and reperfusion injury.

Ischemia and reperfusion injury (IRI) is the main etiology of acute renal failure in native and transplanted kidneys. In the transplantation field, immunosuppressive drugs may play an additional role in acute graft dysfunction. Rapamycin may impair renal regeneration post IRI. Heme oxygenase 1 (HO-1) is a protective gene with anti-inflammatory and anti-apoptotic actions. We investigated whether HO-1 played a role in rapamycin-induced renal dysfunction in an established model of IRI. Rapamycin (3 mg/kg) was administered to mice before being subjected to 45 min of ischemia. Animals subjected to IRI presented with impaired renal function that peaked at 24 h (2.05+/-0.23 mg/dl), decreasing thereafter. Treatment with rapamycin caused even more renal dysfunctions (2.30+/-0.33 mg/dl), sustained up to 120 h after reperfusion (1.54+/-0.4 mg/dl), when compared to the control (0.63+/-0.09 mg/dl, P<0.05). Rapamycin delayed tubular regeneration that was normally higher in the control group at day 5 (68.53+/-2.30 vs 43.63+/-3.11%, P<0.05). HO-1 was markedly upregulated after IRI and its expression was even enhanced by rapamycin (1.32-fold). However, prior induction of HO-1 by cobalt protoporphyrin improved the renal dysfunction imposed by rapamycin, mostly at later time points. These results demonstrated that rapamycin used in ischemic-injured organs could also negatively affect post-transplantation recovery. Modulation of HO-1 expression may represent a feasible approach to limit rapamycin acute toxicity.

Mast cells, TGF-beta1 and myofibroblasts expression in lupus nephritis outcome.

Renal biopsies of 69 patients with lupus nephritis were studied according to the WHO classification. The aim of the present study was to correlate the interstitial tryptase-positive mast cells with the interstitial TGF-beta1 and alpha-SM actin expression and clinical outcome of lupus nephritis, and identify the pathological role of the interstitial tryptase-positive mast cells in lupus nephritis. The mean follow-up time was 70.7 +/- 54.4 months. Eight patients were grouped as WHO class II lupus nephritis, 15 patients as class III, 28 patients as class IV and 18 patients as class V. Interstitial tryptase-positive mast cells were not correlated with clinical outcome and interstitial TGF-beta1 expression in lupus nephritis. Interstitial tryptase-positive mast cells were correlated with tubulo-interstitial alpha-SM actin expression for WHO class V lupus nephritis, but not to the other classes. In conclusion, in spite of interstitial tryptase-positive mast cells being related to renal interstitial fibrosis process, their expression according to the clinical outcome of lupus nephritis was not significant.

Alpha-SM actin expression as prognostic indicator in IgA nephropathy (Berger's disease).

Recent studies have demonstrated that alpha-Smooth Muscle actin expression in glomerular and tubulointerstitial compartments of renal tissue could represent a prognostic marker in several renal diseases. Our objective was to identify the prognostic value of alpha-SM actin actin expression on the evolution of renal damage in Primary IgA nephropathy (Berger's disease). 43 patients followed up from 1988 to 1999 at the University Hospital, Faculty of Medicine of Ribeirão Preto, University of Sao Paulo, Brazil, was studied. Clinical-laboratory data were obtained from the medical records of the patients using a protocol containing name, race, gender, origin, profession, age at clinical presentation of the disease and personal and family history. The parameters assessed in the approach to IgA nephropathy were serum creatinine, creatinine clearance, serum albumin, total serum protein, 24 hours proteinuria, glycaemia, serum sodium, potassium, calcium and phosphorus ions, analysis of urinary sediment, serum complement profile, blood count, and renal biopsy. Morphological evaluation was performed by renal biopsy using common light and immunofluorescence microscopy. Immunohistochemical studies were performed using a murine monoclonal antibody to alpha-SM actin. Our data showed that alpha-SM actin expression in the glomerular and tubulointerstitial compartments are not correlated with unfavorable clinical course of primary IgA nephropathy.

Classes, activity and chronicity indices, and alpha-smooth muscle actin expression as prognostic parameters in lupus nephritis outcome.

Renal biopsies of 86 patients with lupus nephritis were assessed according to the WHO classification, and according to activity and chronicity indices. The aim of the present study was to correlate clinical, and histological features (WHO class, activity and chronicity indices, and alpha-SM actin expression) with the progression of lupus nephritis, and identify the pathological role of alpha-SM actin in lupus nephritis. The median follow-up time was 75.5 +/- 57.3 months. Two patients were grouped as WHO class IIa lupus nephritis, eight patients as class IIb, 16 patients as class III, 25 patients as class IV, 15 patients as class V, and 19 patients as mixed pattern lupus nephritis. Sex, age, race, and the alpha-SM actin expression in glomeruli and tubulo-interstitial area in WHO class III and IV showed no correlation with clinical follow-up outcome of lupus nephritis. Unfavorable clinical outcome of lupus nephritis was correlated with WHO class IV compared to the other classes, and with the chronicity index in WHO class III patients.

Widespread hematogenous metastases and Trousseau's syndrome in gastric adenocarcinoma.

A case of widespread hematogenous metastases and Trousseau's syndrome is reported in a 40 year-old white housewife with gastric cancer, presenting subdural hematoma, ecchymoses, epistaxis, stomach and uterine bleeding. After undergoing hematoma drainage, she was unsuccessfully treated with platelets, red blood cells, plasma cryoprecipitate transfusions, and antibiotics. Necropsy disclosed gastric ring-signet adenocarcinoma invading the serous layer, with massive disseminated intravascular coagulation and systemic neoplastic embolism. Multiple old and recent hyaline (rich in fibrin and platelets) microthrombi, and tumor emboli were observed in the bone marrow, meninges, liver, lungs, kidneys, lymph nodes, adrenals, thyroid, heart, pancreas, and ovaries (Krukenberg tumor).

Morphologic and morphometric evaluation of pancreatic islets in chronic Chagas' disease.

PURPOSE: Hyperglycemia and abnormal glucose tolerance tests observed in some patients with chronic Chagas' disease suggest the possibility of morphological changes in pancreatic islets and/or denervation. The purpose of this study was to describe the morphology and morphometry of pancreatic islets in chronic Chagas' disease. METHODS: Morphologic and computerized morphometric studies were performed in fragments of the head, body, and tail regions of the pancreas obtained at necropsies of 8 normal controls and 17 patients with chronic Chagas' disease: 8 with the digestive form (Megas) and 9 with the congestive heart failure form. RESULTS: The Megas group had a larger (p < 0.05) pancreatic islet area in the tail of the pancreas (10649.3 +/- 4408.8 micrometer2) than the normal control (9481.8 +/- 3242.4 micrometer2) and congestive heart failure (9475.1 +/- 2104.9 micrometer2) groups; likewise, the density of the pancreatic islets (PI) was greater (1.2 +/- 0.7 vs. 0.9 +/- 0.6 vs. 1.9 +/- 1.0 PI/mm2, respectively). In the tail region of the pancreas of patients with the Megas form, there was a significant and positive correlation (r = +0.73) between the area and density of pancreatic islets. Discrete fibrosis and leukocytic infiltrates were found in pancreatic ganglia and pancreatic islets of the patients with Chagas' disease. Trypanosoma cruzi nests were not observed in the examined sections. Individuals with the Megas form of Chagas' disease showed increased area and density of pancreatic islets in the tail of the pancreas. CONCLUSION: The observed morphometric and morphologic alterations are consistent with functional changes in the pancreas, including glycemia and insulin disturbances.

[Contribution to the morphologic diagnosis of lung adiaspiromycosis]. / Contribuição ao diagnóstico morfológico da adiaspiromicose pulmonar.

The diagnosis of adiaspiromycosis is usually based on lung sections stained by hematoxylin-eosin, periodic acid Schiff and methenamine silver. Authors describe the fungus aspect examined by mucicarmin, picro-sirius and Congo red methods, including polarized light microscopy. In doubtful cases, these methods could contribute to histopathological diagnosis of Emmonsia parva var crescens.

[Human accidents with stings from Africanized bees]. / Acidente humano por picadas de abelhas africanizadas.

It is report five cases of stings of africanized bees (AB). Four of them were victims of multiple stings, varying from 25 to 60, that presented severe headache, nauseas and vomits, related to the clinic effect of the toxicity of the venom, with good evolution. The other case was victim of a single sting of AB and died after probable anaphylaxis.

[Clinical and laboratory renal alterations in patients with acquired immunodeficiency syndrome in relation to anatomopathological findings]. / Alterações renais clínico-laboratoriais em pacientes com a síndrome da imunodeficiência adquirida em relação aos achados anatomopatológicos.

Clinical as well as renal anatomopathological data of 119 patients with acquired immunodeficiency syndrome from the Hospital of the Faculty of Medicine of Triângulo Mineiro, Uberaba, MG, Brazil, were studied. Mean age was 33 +/- 10.4 years (range 18 to 67 years). White (59%) and male (80%) individuals predominated. Ninety percent of patients came from Uberaba or neighborhood. There were 59 (50%) heterosexual, 25 (21%) homosexual, 17 (14%) bisexual and 18 (15%) unknown. Forty three percent were drug abusers. Fourteen (12.2%) of patients had serum creatinine higher than 3mg/dl, ten days before death, 64% of them showed acute tubular necrosis. Seventy one (61%) patients presented hyponatremia and 8 (7%) had hypernatremia. Hypokalemia was detected in 28 (24%) and hyperkalemia in 8 (7%) patients. Twenty four hours urinary protein was detected in 12 patients, 7 of them presenting more than 1g/24h. Two patients showed segmentar focal glomerulosclerosis, one of them with 24h urinary protein level of 5.5 g and serum creatinine 1.5 mg/dl and no edema. The most (56%) patients had tubulointerstitial nephritis. Clinical, laboratory and types of renal disorders in patients with acquired immunodeficiency syndrome are variable. The glomerular diseases were relatively scarce however, tubulointerstitial lesions are quite frequent, mainly interstitial nephritis and acute tubular necrosis. Not always an anatomoclinical correlation could be observed, because many times the electrolyte disorders were frequently observed only functionally.

[Systemic talc granulomatosis in a HIV-negative intravenous drug addict]. / Correlação anátomo-clínica: granulomatose sistêmica por talco em drogadicto HIV negativo.

Anatomo-pathological correlation in a case of systemic talc granulomatosis affecting lungs, pleura, liver, spleen and mesenteric lymph nodes resulting in pulmonary arterial hypertension and cor pulmonale is described. The patient, a 26-year-old male HIV-negative intravenous drug addict had no lymphopenia or any histopathologic findings at necroscopy compatible with AIDS, despite of a chronic high-risk behavior favoring this illness.

[The weight of the spleen in chronic chagasics]. / O peso do baço em chagásicos crônicos.

During the course of systemic inflammatory reactions and chronic venous congestion, the documented phenomenon of increased spleen size is respectively called reactional hyperplasia and congestive splenomegaly. In Chagas' disease, the inflammatory process observed in the heart of chronically infected patients can result in heart failure and ultimately in congestive failure. In order to evaluate the spleen response to both inflammatory and cardiac processes, in this retrospective study we compare the weight of spleens from normal and chagasic patients, with or without congestive failure. Information about patient age, sex, race and spleen weight was collected from autopsy reports. Eighty-eight selected cases were divided into four groups: 1) chagasic patients with congestive failure, 2) chagasic patients without congestive failure, 3) non-chagasic patients with congestive failure, 4) non-chagasic patients without congestive failure. The average age was 44.9 +/- 15.4 years, 53.4% were Caucasians and 70.5% were males, and no significant difference in these parameters was observed between the four groups. The spleen weight for the groups presenting congestive failure was 183.7 +/- 85.9 g for chagasic and 206.3 +/- 101.0 g for non-chagasic patients; for the groups without congestive failure the average spleen weight was 173.7 +/- 118.9 g for the chagasic and 117.2 +/- 52.0 g for non-chagasic patients. The spleen weight was significantly higher for the chagasic patients without congestive failure when compared to the non-chagasic group without congestive failure. These results suggest that the inflammatory component in Chagas' disease plays an important role in the increase of spleen weight together with hemodynamic alterations arising from congestive heart failure.