Benign prostatahyperplasi (BPH) är en av de vanligaste sjukdomarna hos män och kan vara en orsak till lidande. Hur omfattande lidandet är hos dem som drabbas är individuellt. Studiens syfte var att belysa patienters lidande vid BPH. En systematisk litteraturstudie valdes som metod. Sökning i relevanta databaser; Cinahl, PubMed, PsycINFO och ELIN@Kalmar, utfördes och därefter följde kritisk granskning, dataanalys och sammanställning av vetenskapligt material inom problemområdet. I dataanalysen framkom tre teman: fysiskt, emotionellt samt sexuellt lidande. Det fanns rädsla för prostatacancer och för att vara beroende av andra. En annan typ av rädsla gällde urinläckage som syntes utåt. Förändrade miktionsvanor upplevde patienter som pinsamma. Vanliga symtom vid BPH var svag urinstråle, urinläckage samt frekventa toalettbesök. Genom en gruppkonstellation av patienter, urologer och anhöriga där erfarenheter kunde utbytas, underlättades det fortsatta livet med sjukdomen. Trots allt fanns en acceptans och uppfattning om att sjukdomen är en naturlig del av åldrandet. För att kunna agera stödjande till patienter med BPH bör sjuksköterskan initiera till samtal med patienten utan att negligera de sexuella funderingar patienten eventuellt kan ha. Att anordna gruppmöten så att patienter kan utbyta erfarenheter med varandra kan vara värdefullt.

<p>Benign prostatahyperplasi (BPH) är en av de vanligaste sjukdomarna hos män och kan vara en orsak till lidande. Hur omfattande lidandet är hos dem som drabbas är individuellt. Studiens syfte var att belysa patienters lidande vid BPH. En systematisk litteraturstudie valdes som metod. Sökning i relevanta databaser; Cinahl, PubMed, PsycINFO och ELIN@Kalmar, utfördes och därefter följde kritisk granskning, dataanalys och sammanställning av vetenskapligt material inom problemområdet. I dataanalysen framkom tre teman: fysiskt, emotionellt samt sexuellt lidande. Det fanns rädsla för prostatacancer och för att vara beroende av andra. En annan typ av rädsla gällde urinläckage som syntes utåt. Förändrade miktionsvanor upplevde patienter som pinsamma. Vanliga symtom vid BPH var svag urinstråle, urinläckage samt frekventa toalettbesök. Genom en gruppkonstellation av patienter, urologer och anhöriga där erfarenheter kunde utbytas, underlättades det fortsatta livet med sjukdomen. Trots allt fanns en acceptans och uppfattning om att sjukdomen är en naturlig del av åldrandet. För att kunna agera stödjande till patienter med BPH bör sjuksköterskan initiera till samtal med patienten utan att negligera de sexuella funderingar patienten eventuellt kan ha. Att anordna gruppmöten så att patienter kan utbyta erfarenheter med varandra kan vara värdefullt.</p>

Magister Scientiae (Medical Bioscience) - MSc(MBS) / The prostate is prone to three pathological processes that include inflammation, benign prostate hyperplasia (BPH) and tumors. According to the center for Disease and Control 1999-2012 report, prostate cancer is the second leading cause of death in the United States. Scientific evidence suggests that up to 30% of men in the general population aged from 50 years and above, irrespective of geographic origin, have foci of prostate neoplastic growth. Unbalanced ROS production and a dysregulated antioxidant defence system have been implicated in prostate cancer development. The transformation of a normal cell into cancer takes a very long period. This observation provides the advantage of using nutraceuticals to prevent, arrest or reverse the cellular and molecular processes of carcinogenesis. Based on scientifically observed positive health roles of green tea (Cameli sinensis) and rooibos (Aspalathus linearis) on major diseases like atherosclerosis, hepatitis and certain types of cancer, this thesis evaluated the effects of these two teas on benign (RPWE 1) and malignant (LNCaP) prostate cells. This was done through the quantification of reactive oxygen species (ROS) using a fluorescence dye 5,6 CM-H2DCFDA, total prostate specific antigen (PSA) levels using a PSA ELISA kit, cell viability using the MTT assay, apoptosis using Tali annexin V stain and cell imaging studies using a Zeiss axiovert 200M inverted fluorescence microscope. Statistical analysis was done using graphpad prism. The findings of this study show that aqueous extracts of green and black tea, fermented and unfermented rooibos and their active compounds epigallocatechin gallate (EGCG) and aspalatin, respectively, are cytotoxic in malignant (LNCaP) prostate cells but exert protective effects in benign (RPWE 1) prostate cells. This thesis implicates the pro-oxidant and anti-oxidant properties of the plant extracts, respectively, for the above mentioned effects. In this regard, tea and rooibos promoted ROS production in malignant (LNCaP) prostate cells, which subsequently promoted cell death of the malignant cells through apoptosis and necrosis. Further to this, tea and rooibos used in this thesis, protected normal prostate cells from the adverse effects of ROS. In this regard, fluorescence microscope photographs showed RPWE 1 cells with low DCF fluorescence compared to the malignant prostate cells. Low magnification light microscope photographs showed RPWE 1 cells with flat polygonal shapes and increased adherence both at low and high concentrations of tea and rooibos. On the contrary, high concentrations of tea and rooibos on malignant (LNCaP) prostate cells induced stress, which made the cells attain irregular shapes and as the stress levels increased, cells became detached and appeared dead. Flow cytometry confirmed the presence of apoptotic and necrotic cell in malignant (LNCaP) prostate cells. In this thesis, EGCG and aspalathin were responsible for the high rates of apoptosis observed whereas green tea and unfermented rooibos induced the highest rate of necrosis. Further to this, tea and rooibos and the main active compounds EGCG and aspalathin, respectively, significantly promoted the reduction of total serum prostate specific antigen (PSA) in malignant prostate cells. In normal prostate cells, these plant extracts maintained the total serum PSA at its basal physiological level. In this thesis, to the best of our knowledge, we report for the first time the cell-specific effects of fermented rooibos, unfermented rooibos and their main active component aspalathin, on prostate cancer cells. We showed that rooibos and aspalathin exert pro-oxidant effects on malignant LNCaP cells and anti-oxidant effects on benign RPWE 1 cells. In conclusion, tea (C. sinensis) and rooibos (A. linearis) and their respective main active compounds, epigallocatechin gallate and aspalathin, are cytotoxic to malignant prostate cells whereas in normal prostate cells, they have protective effects against ROS induced stress. The pro-oxidant and anti-oxidant effects are responsible for the aforementioned effects respectively. The decrease in total serum PSA demonstrate the strong therapeutic effects that tea and rooibos have on malignant (LNCaP) prostate cells. / Malawi Government: Department of Human Resources Development and Management

Prostasin is expressed in normal prostate epithelial cells but down-regulated in prostate cancers, while prostasin re-expression in invasive prostate cancer cells reduced invasion. We examined prostasin expression and function in benign prostatic hyperplasia (BPH). We evaluated prostasin expression in 12 BPH specimens by immunohistochemistry, and evaluated the impact of prostasin silencing by siRNA on the expression of the inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1), and cyclin D1, as well as on cell proliferation and invasion, using the BPH-1 human prostate epithelial cell line model. Prostasin expression was localized in the glands of BPH tissues by immunohistochemistry, in either the tall columnar-shaped or the flattened epithelial cells. We silenced prostasin expression by >50% at both the mRNA and protein levels using siRNA in the BPH-1 human prostate epithelial cell line, and this silencing of prostasin expression was associated with an induction of iNOS and ICAM-1 expression and a down-regulation of cyclin D1 expression. The protein expression of EGFR, a putative prostasin substrate, was not affected by prostasin silencing in this cell line. The prostasin-silenced cells displayed a reduced cell proliferation rate and reduced invasiveness, cell behaviors regulated by cyclin D1, iNOS, and ICAM-1 in the BPH-1 cells. We believe that this down-regulation of cyclin D1 is due to prostasin's augmentative effect on iNOS. We also believe that the decrease in cell motility is due to an increase in iNOS and ICAM-1 as well as a decrease in cyclin D1, since all of these molecules can play a role in cell motility. In conclusion, Prostasin is somehow involved in the regulation of inflammatory gene expression (iNOS and ICAM-1) in prostate epithelial cells, as well as cyclin D1 expression, cell proliferation and invasion, involving molecular mechanisms different than those in the prostate cancer cells. These studies suggest that prostasin is a player in the glandular components of benign prostatic hyperplasia.

In the first part of this thesis is discussed of the possibilities of surface grinding. There are described various methods for grinding and describe their characteristics. Furthermore, there is shown the marking of grinding wheels and is discussed of their composition and of calculating the cutting forces. In the second part of this thesis the experiment is performed. On the samples of various materials are monitored parameters of roughness after grinding, which is used by conventional grinding BPH 300 and horizontal lathe from company TDZ Turn.

In spite of the fact that prostate cancer is the most common male cancer in both Sweden and many other countries in the developed world, little is known of risk factors and predisposing conditions. The only well recognized risk factors are age, race and familial aggregation. More knowledge about risk factors could lead to better preventive measures together with better treatments. One way to evaluate this is to study second primary cancers; the connection between two different cancers can give valuable insight in etiology or clues to shared risk factors. This thesis aims at evaluating risk factors for prostate cancer. We constructed a cohort of 135,713 men diagnosed with prostate cancer and reported to the Swedish Cancer Registry 1958-1996. The cohort was followed for second primary cancers and a doubled risk of male breast cancer was found. We also noted increased risks for small intestine cancers and melanoma. As a follow-up on the increased risk of male breast cancer, we performed a nested case – control study. Included cases were men with first prostate and then breast cancer (n = 41) matched to men with only prostate cancer (n =81). For these men, we collected medical records and extracted data regarding treatment. Furthermore, all men diagnosed with both prostate and breast cancer irrespective which came first (n = 83) were used as probands. To both these sets of cases with breast and prostate cancer, we identified first degree relatives and grandchildren from parish offices throughout Sweden. Linking to the Cancer Registry retrieved all cancer diagnoses amongst relatives. Results from this study show a relation between estrogen treatment of prostate cancer and the risk of developing breast cancer. We also found that a small part of the cases with both cancers appeared in families with inheritance patterns possibly attributed to BRCA2. As estrogen treatment seemed involved in increased risk of breast cancer after prostate cancer, we wanted to investigate the newly discovered Estrogen receptor β and the relation to prostate cancer risk. Previous reports have shown that ERβ acts as a negative regulator of proliferation. ERβ expression occurs mainly in prostatic epithelial cells and the expression gradually diminishes when cancer develops and aggravates. We used a single nucleotide polymorphism (SNP) association study approach to evaluate genetic variation in ERβ as a risk factor for prostate cancer. One SNP, located in the promoter region associated with a small increased risk of prostate cancer whereas variation in the rest of the gene did not. In the last paper, we investigated trans-urethral resection (TURP) of the prostate due to benign prostate hyperplasia (BPH) as a risk factor for later development of prostate cancer. Evidence has gathered that both BPH and prostate cancer are associated to inflammation. By comparing incidence and mortality in a cohort of 7,901 men with the general population there appeared to be an increased risk of prostate cancer but decreased mortality. Analyzing this increased risk further, we conducted a nested case - control study with men extracted from the cohort. Cases had a TURP and later developed prostate cancer and controls just had a TURP. We then evaluated the specimens from TURP regarding extent of inflammation, degree of androgen receptor down regulation and expression of p53, all factors previous associated with prostate cancer. None of these parameters differed between cases and controls and they can therefore not explain the increased risk. Decreased mortality but increased risk might be explained by surveillance bias, which means more medical attention to these patients, resulting in diagnosing clinically non-significant cancers. In summary, our results show a doubled risk of male breast cancer following prostate cancer. A risk that can be attributed to the use of estrogen to treat prostate cancer or to some extent a possible mutation in BRCA2. We also propose that a SNP change in the ERβ promoter confer a small increased risk of prostate cancer. A small risk elevation of prostate cancer following TURP most probable could depend on surveillance bias.

No description available.

Prostate cancer is one of the most common malignant tumors in solid organs of old men. However, the patients are nearly 100 percent survivable if detected early. Prostate-specific antigen (PSA) is a valuable prostate cancer biomarker that is now wildly used for population screening, diagnosis, and monitoring of patients with prostate cancer. But PSA is not good enough for a biomarker because it can not distinguish benign prostate hyperplasia (BPH) from prostate tumor . Recently, there are some tumor marker still in study, for example: free prostate specific antigen¡]fPSA), complexed prostate specific antigen (C-PSA), kallikrein,prostate specific membrane antigen (PSMA). From previously study,we had found many different protein expressions between serum of normal and prostate patients. Mayven is one of the novel proteins that had been identified. The mRNA expression of Mayven in prostate cancer tissue is determined by quantitative RT-PCR. The result shows that the mRNA expression of Mayven in Benign Prostatic Hyperplasia (BPH) is about 5.0-11.3 fold than normal tissue , 12.7 fold in Prostate Cancer (PCa) stage T1 and 0.1- 3.7 fold after cancer stage T2. The Mayven gene expression is predominate in tumor stage T1, decrease after T2 stage. However the expressed pattern of mayven in BPH remains further investigation due to the limited sample size. Furthermore, with 2 dimensional electrophoresis (2¡VDE), we have found 7 differentially expressed proteins between tissue of normal and prostate patients, and these proteins are identified by MALDI-TOF mass spectrometry and MS-Fit. These identified proteins are Keratin 8¡]KRT8¡^, MAPKkinase5¡]MAP2K5¡^, Acid phosphatase (ACPP), Annexin A3¡]ANXA3¡^, Phosphoglycerate mutase 1 (PGAM1), Spindlin-like protein 2 (SPIN2) and Transgelin 2¡]TAGLN2¡^.

No description available.

Made available in DSpace on 2014-07-29T15:07:55Z (GMT). No. of bitstreams: 1 dissertacao mariana faleiro part 1.pdf: 60728 bytes, checksum: 82e5bf30cd60c4752f1de660f88797ed (MD5) Previous issue date: 2010-03-02 / Humans and dogs show dysplastic lesions in the prostate, such as prostatic intraepithelial neoplasms (PIN) and proliferative inflammatory atrophy (PIA), which are studied due to their malignance potential. The matrix metalloproteinases (MMP) are a family of proteolytic enzymes thought to play an important role in tumor invasion and metastasis in face of their ability to degrade the extracellular matrix (ECM) and basement membrane. The plasminogen activator (PA) system has been suggested to play a central role in cell adhesion, migration, wound healing, angiogenesis, inflammation, regulation of growth factors and tumor invasion. The receptor of plasminogen activator type activator (uPAR) is a component of the PA, with a range of expression in tumor cell and stromal cells. So, this study was aimed to evaluated the expression and correlation between MMP-2 (gelatinase A) and MMP-9 (gelatinase B) as well as the expression of uPAR in normal canine prostate tissue and also in tissue with proliferative disorders, including benign prostatic hyperplasia (HPB), PIA, PIN and carcinoma. And therefore establish relation among the role of these enzymes in the remodeling of the extracellular matrix (ECM) and in the process of tumor invasion and metastasis. For this, it was performed immunohistochemical staining in tissue microarray of 149 paraffin-embedded fragments of prostate tissue selected from 57 prostates of non-castrated adult dogs with or without prostatic diseases. A total of 298 cores were analyzed and it was made 363 diagnoses: 36 (9.9%) normal, 49 (13.5%) BPH, 132 (36.3%) PIA, 75 (20.7%) PIN and 71 (19.6%) carcinomas. It was observed differences in cytoplasmatic immunohistochemical staining by MMP-2 and MMP-9 antibodies in relation to the cell number and intensity of labeling of the acinar epithelial and stromal perilobular cells between normal tissue and in those with proliferative disorders. A correlation between MMP-2 and MMP-9 antibodies occurred just in canine prostates with PIA in relation to the number of labeled cells in acinar epithelium and perilobular stroma, as well as, the staining intensity in the perilobular stromal cells. In relation to uPAR, it was observed differences of immunohistochemical staining of uPAR antibodies in canine prostate. Likewise, there was over expression in dysplastic and neoplasic specimens, but not in normal and benign prostate tissue. A number of epithelial cells labeled for uPAR showed variation among the diagnoses, except between PIN and carcinoma. Less intensity of labeling was observed in acinar epithelial cells of normal prostates compared with PIA, PIN and carcinoma. However, in the normal cells and in those with PIA, there was a difference in the number of cells, as well as in the intensity of stromal labeling. The intensity of labeling of stromal perilobular cells was higher in the PIA. PIA-A (accentuated) and PIA-M (moderated) cells showed greater intensity staining stroma and stromal cells labeled for uPAR, respectively. Thus, this study concludes that there was variation in gelatinases and uPAR expression in canine prostate according to the lesion. Also, there was Less labeling in normal and BPH and higher in PIA, PIN and carcinoma prostate tissues. The correlation between MMP-2 and MMP-9 in canine prostates with PIA indicates that the inflammation likely influenced the activity of these enzymes with simultaneous increase in their expression. The uPAR high expression in inflammatory and neoplasic tissues suggests high ECM proteolytic activity in these situations / Nas espécies humana e canina lesões displásicas da próstata, como a neoplasia intra-epitelial prostática (PIN) e a atrofia inflamatória proliferativa (PIA), são estudadas quanto ao potencial de malignidade. As metaloproteinases (MMP) são enzimas proteolíticas envolvidas no processo de invasão tumoral e metástase, causando destruição de barreiras biológicas como a matriz extracelular (MEC) e a membrana basal (MB). O sistema ativador de plasminogênio (PA) compreende proteínas com ação na adesão celular, regulação da migração, cicatrização, angiogênese, inflamação, regulação de fatores de crescimento e invasão tumoral. O receptor de ativador de plasminogênio tipo uroquinase (uPAR) é um dos componentes do PA, com variação de expressão em células neoplásicas e estromais. Este trabalho teve por objetivo verificar a expressão e a correlação entre MMP-2 e MMP-9, assim como a expressão do uPAR no tecido prostático canino normal e com alterações proliferativas, incluindo a hiperplasia prostática benigna (HPB), a PIA, a PIN e o carcinoma, buscando avaliar o papel dessas proteínas no remodelamento da MEC e no processo de invasão tumoral e metástase. Para isso, foi realizada a imunoistoquímica em lâminas de microarranjo tecidual (TMA), com 149 cores selecionadas de 57 próstatas de cães adultos, não castrados, com ou sem histórico de afecções prostáticas. Foram analisados, para cada anticorpo, 298 cores, perfazendo 363 diagnósticos, sendo 36 (9,9%) normais, 49 (13,5%) HPB, 132 (36,3%) PIA, 75 (20,7%) PIN e 71 (19,6%) carcinomas. Foi possível observar diferença de imunomarcação citoplasmática de MMP-2 e MMP-9 em relação ao número de células e intensidade de imunomarcação nas células epiteliais acinares e estromais periacinares em relação aos diagnósticos. A correlação entre os anticorpos MMP-2 e MMP-9 ocorreu em próstatas caninas com PIA quanto ao número de células imunomarcadas no epitélio acinar e no estroma periacinar, bem como quanto à intensidade de imunomarcação nas células estromais periacinares. Quanto ao uPAR, houve diferença na imunomarcação em relação ao diagnóstico, com maior expressão nas displásicas e neoplásicas em relação ás normais e com HPB. O número de células epiteliais imunomarcadas para uPAR variou entre os diagnósticos, exceto entre PIN e carcinoma. Menor intensidade de imunomarcação epitelial foi constatada nas próstatas normais em relação às com PIA, PIN e carcinoma. Entre as normais e com PIA houve diferença no número de células e intensidade de imunomarcação estromal. A intensidade de imunomarcação estromal foi maior nas com PIA. As PIA-M (inflamação moderada) e PIA-A (inflamação acentuada) apresentaram maior intensidade de imunomarcação estromal e células estromais imunomarcadas para uPAR, respectivamente. Concluiu-se que há variação na expressão das gelatinases e do uPAR na próstata canina, de acordo com a lesão, com menor expressão nas normais e com HPB e maior naquelas com PIA, PIN e carcinoma. A correlação entre MMP-2 e MMP-9 em próstatas caninas com PIA indica que a inflamação influencia a atividade dessas enzimas, com aumento simultâneo na expressão de ambas no microambiente inflamatório. Ainda, o aumento na expressão do uPAR nos microambientes inflamatório e neoplásico sugere maior atividade proteolítica na MEC nesses casos