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  • 1.
    Braide, Magnus
    et al.
    Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Göteborg, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Waniewski, Jacek
    Institute of Biocybernetics and Biomedical Engineering, Polish Academy of Sciences, Warsaw, Poland.
    Erythrocytes as volume markers in experimental pd show that albumin transport in the extracellular space depends on pd fluid osmolarity2016Ingår i: Peritoneal Dialysis International, ISSN 0896-8608, E-ISSN 1718-4304, Vol. 36, nr 3, s. 247-256Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Macromolecules, when used as intraperitoneal volume markers, have the disadvantage of leaking into the surrounding tissue. Therefore, Cr-51-labeled erythrocytes were evaluated as markers of intraperitoneal volume and used in combination with I-125-labeled bovine serum albumin to study albumin transport into peritoneal tissues in a rat model of peritoneal dialysis (PD).

    Methods: Single dwells of 20 mL of lactate-buffered filter-sterilized PD fluid at glucose concentrations of 0.5%, 2.5%, and 3.9% were performed for 1 or 4 hours. Tissue biopsies from abdominal muscle, diaphragm, liver, and intestine, and blood and dialysate samples, were analyzed for radioactivity.

    Results: The dialysate distribution volume of labeled erythrocytes, measured after correction for lymphatic clearance to blood, was strongly correlated with, but constantly 3.3 mL larger than, drained volumes. Erythrocyte activity of rinsed peritoneal tissue biopsies corresponded to only 1 mL of dialysate, supporting our utilization of erythrocytes as markers of intraperitoneal volume. The difference between the distribution volumes of albumin and erythrocytes was analyzed to represent the albumin loss into the peritoneal tissues, which increased rapidly during the first few minutes of the dwell and then leveled out at 2.5 mL. It resumed when osmotic ultrafiltration turned into reabsorption and, at the end of the dwell, it was significantly lower for the highest osmolarity PD fluid (3.9% glucose). Biopsy data showed the lowest albumin accumulation and edema formation in abdominal muscle for the 3.9% fluid.

    Conclusion: Labeled erythrocytes are acceptable markers of intraperitoneal volume and, combined with labeled albumin, provided novel kinetic data on albumin transport in peritoneal tissues.

  • 2.
    Delbro, Dick
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Hallsberg, Lena
    Department of Surgery, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Peeker, Ralph
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy. University of Gothenburg, Gothenburg, Sweden.
    Scherbak, Nikolai
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Fall, Magnus
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Godtman, Rebecka Arnsrud
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    The extracellular matrix-degrading protein ADAMTS5 is expressed in the nuclei of urothelial cells in healthy rats2018Ingår i: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 52, nr 2, s. 139-142Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: The aim of this study was to investigate whether protein expression of the extracellular matrix-degrading protease ADAMTS5 can be demonstrated in the urinary bladder of healthy rats, and, if so, to determine the localization of this enzyme.

    MATERIALS AND METHODS: The experiments were conducted with eight inbred male Sprague-Dawley rats. Immunohistochemistry was used to investigate the expression of ADAMTS5 in the urinary bladder. Negative controls were established by either excluding the primary antibody or applying the antibody after it had been preabsorbed with its immunogenic peptide. Confocal microscopy was used to visualize the distribution of ADAMTS5 in the urinary bladder tissue.

    RESULTS: Immunoreactivity for ADAMTS5 was demonstrated in the urothelium and in the detrusor. This expression was localized not only in the cytoplasm, but also in the nuclei. Confocal microscopy corroborated these findings.

    CONCLUSION: Expression of ADAMTS5 was demonstrated in the cytoplasm as well as in the nuclei of the urothelium and detrusor cells, suggesting that it may play a role at the transcriptional level.

  • 3.
    Engström, Alexander
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Erlandsson, Ann
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Conditioned media from macrophages of M1, but not M2 phenotype, inhibit the proliferation of the colon cancer cell lines HT-29 and CACO-22014Ingår i: International Journal of Oncology, ISSN 1019-6439, Vol. 44, nr 2, s. 385-392Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Solid tumors are infiltrated by stroma cells including macrophages and these cells can affect tumor growth, metastasis and angiogenesis. We have investigated the effects of conditioned media (CM) from different macrophages on the proliferation of the colon cancer cell lines HT-29 and CACO-2. CM from THP-1 macrophages and monocyte-derived human macrophages of the M1 phenotype, but not the M2 phenotype, inhibited proliferation of the tumor cells in a dose-dependent manner. Lipopolysaccaharide and interferon gamma was used for differentiation of macrophages towards the M1 phenotype and CM were generated both during differentiation (M1(DIFF)) and after differentiation (M1). M1 and M1(DIFF) CM as well as THP-1 macrophage CM resulted in cell cycle arrest in HT-29 cells with a decrease of cells in S phase and an increase in G(2)/M phase. Treatment of HT-29 cells with M1(DIFF), but not M1 or THP-1 macrophage CM, resulted in apoptosis of about 20% of the tumor cells and this was accompanied by lack of recovery of cell growth after removal of CM and subsequent culture in fresh media. A protein array was used to identify cytokines released from M1 and M2 macrophages. Among the cytokines released by M1 macrophages, tumor necrosis factor alpha and CXCL9 were tested by direct addition to HT-29 cells, but neither affected proliferation. Our results indicate that M1 macrophages inhibit colon cancer cell growth and have the potential of contributing to reducing tumor growth in vivo.

  • 4.
    Godtman, Rebecka Arnsrud
    et al.
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Hallsberg, Lena
    Department of Surgery, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Löf-Öhlin, Zarah
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. The Clinical Research Laboratory.
    Peeker, Ralph
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för medicinska vetenskaper.
    The extracellular matrix proteoglycan versican is strongly expressed in the urothelium of healthy rats2019Ingår i: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 53, nr 6, s. 431-434Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: We have previously demonstrated protein expression of the extracellular matrix degrading protein ADAMTS5 in the nuclei of urothelial cells in healthy rats. The proteoglycan versican constitutes one of the main substrates for this protease. In this follow up study we investigated a potential co-localization of versican and ADAMTS5 in the urinary bladder wall.

    Material and Methods: The study was conducted with archive material (paraffin embedded bladder tissue from our previous study, i.e., 8 male Sprague-Dawley rats). Protein expression of versican was investigated by immunohistochemistry. Furthermore, the occurrence of versican mRNA was examined by in-situ hybridization.

    Results: Positive immunoreactivity for versican was evident in the urothelium but also, weakly, in the detrusor. This expression was localized only in the cytoplasm, leaving the nuclei devoid of reactivity. Interestingly, versican mRNA was only sparsely observed in the urothelial cells.

    Conclusions: We found by immunohistochemistry that the substrate for ADAMTS5, versican, was localized in the cytosol of urothelial cells. This demonstrates a difference regarding the expression of ADAMTS5, which was emphasized in the nuclei. This could imply an additional, non-enzymatic, function of ADAMTS5 in the urothelium.

  • 5.
    Hedbrant, Alexander
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Erlandsson, Ann
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Conditioned media from human macrophages of M1 phenotype attenuate the cytotoxic effect of 5-fluorouracil on the HT-29 colon cancer cell line2015Ingår i: International Journal of Oncology, ISSN 1019-6439, Vol. 46, nr 1, s. 37-46Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Resistance of tumor cells to chemotherapy, such as 5-fluorouracil (5-FU), is an obstacle for successful treatment of cancer. As a follow-up of a previous study we have investigated the effect of conditioned media (CM) from macrophages of M1 or M2 phenotypes on 5-FU cytotoxicity on the colon cancer cell lines HT-29 and CACO-2. HT-29 cells, but not CACO-2 cells, having been treated with a combination of M1 CM and 5-FU recovered their cell growth to a much larger extent compared to cells having been treated with 5-FU alone when further cultured for 7 days in fresh media. M1 CM treatment of HT-29, but not CACO-2 cells, induced cell cycle arrest in the G(0)/G(1) and G(2)/M phases. 5-FU treatment induced accumulation of cells in S-phase in both HT-29 and CACO-2 cells. This accumulation of cells in S-phase was attenuated by combined M1 CM and 5-FU treatment in HT-29 cells, but not in CACO-2 cells. The mRNA expression of cell cycle regulatory proteins and 5-FU metabolic enzymes were analyzed in an attempt to find possible mechanisms for the M1 CM induced attenuation of 5-FU cytotoxicity in HT-29. Thymidylate synthetase (TS) and thymidine phosphorylase (TP) were found to be substantially downregulated and upregulated, respectively, in HT-29 cells treated with M1 CM, making them unlikely as mediators of reduced 5-FU cytotoxicity. Among cell cycle regulating proteins, p21 was induced in HT-29 cells, but not in CACO-2 cells, in response to M1 CM treatment. However, small interfering RNA (siRNA) knockdown of p21 had no effect on the M1 CM induced cell cycle arrest seen in HT-29 and neither did it change the growth recovery after combined treatment of HT-29 cells with M1 CM and 5-FU. In conclusion, treatment of HT-29 cells with M1 CM reduces the cytotoxic effect of 5-FU and this is mediated by a M1 CM induced cell cycle arrest in the G(0)/G(1) and G(2)/M phases. So far, we lack an explanation why this action is absent in the CACO-2 cells. The current findings may be important for optimization of chemotherapy in colon cancer.

  • 6.
    Hedbrant, Alexander
    et al.
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Seidal, Tomas
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Erlandsson, Ann
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Macrophages of M1 phenotype have properties that influence lung cancer cell progression2015Ingår i: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, nr 11, s. 8715-8725Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Stromal macrophages of different phenotypes can contribute to the expression of proteins that affects metastasis such as urokinase-type plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor-1 (PAI-1), but knowledge of how essential their contribution is in comparison to the cancer cells in small cell lung cancer (SCLC) and lung squamous cell carcinoma (SCC) is lacking. The expression of uPA, uPAR, and PAI-1 and of the matrix metalloproteinases (MMP)-2 and MMP-9 were studied in human macrophages of M1 and M2 phenotype and compared to a lung SCC (NCI-H520) and a SCLC (NCI-H69) cell line. Effects of treatment with conditioned media (CM) from M1 and M2 macrophages on the expression of these genes in H520 and H69 cells as well as effects on the cell growth were investigated. In addition, data on the stromal macrophages immunoreactivity of uPAR, MMP-2, and MMP-9 in a few SCC and SCLC biopsies was included. uPAR, MMP-2, and MMP-9 were confirmed in stromal cells including macrophages in the SCC and SCLC biopsies. In vitro, both macrophage phenotypes expressed considerably higher mRNA levels of uPA, uPAR, PAI-1, and MMP-9 compared to the cancer cell lines, and regarding uPAR, the highest level was found in the M1 macrophage phenotype. Furthermore, M1 CM treatment not only induced an upregulation of PAI-1 in both H520 and H69 cells but also inhibited cell growth in both cell lines, giving M1 macrophages both tumor-promoting and tumor-killing potential.

  • 7.
    Hultén, Leif
    et al.
    Sahlgrenska University Hospital, Gothenburg, Sweden.
    Angerås, U.
    Sahlgrenska University Hospital, Gothenburg, Sweden.
    Scaglia, M.
    S. Luigi Gonzaga University Hospital, Orbassano, Turin, Italy.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Sacral nerve stimulation (SNS), posterior tibial nerve stimulation (PTNS) or acupuncture for the treatment for fecal incontinence: a clinical commentary2013Ingår i: Techniques in Coloproctology, ISSN 1123-6337, E-ISSN 1128-045X, Vol. 17, nr 5, s. 589-592Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Sacral nerve stimulation (SNS) has become an established therapy worldwide for the treatment for fecal incontinence. A large number of papers have been published over the years, and SNS is generally considered very effective with improved continence and quality of life for most patients. However, the results are mostly expressed in the semi-quantitative terms, that is, patients' diaries translated into score points. The clinical value of SNS is questionable, especially as the patient groups are usually small and/or etiologically heterogenic and the follow-up period mostly short. The Health Technology Assessment organization in the west region of Sweden has recently evaluated the SNS with regard to evidence, efficacy and risks. Economic and ethical aspects raise serious questions on this expensive and not entirely risk-free treatment in routine medical care. Similar criticism has also been raised by other reviewers proposing a more thorough scientific assessment with well-designed randomized trials and comparison with other similar methods of treatment.

  • 8.
    Lindsten, Therése
    et al.
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Hedbrant, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Ramberg, Anna
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; School of Medical Sciences, Örebro University, Örebro, Sweden.
    Wijkander, Jonny
    Department of Health Sciences, Karlstad University, Karlstad, Sweden.
    Solterbeck, Anja
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden.
    Eriksson, Margareta
    Department of Clinical Pathology and Cytology, Central Hospital Karlstad, Karlstad, Sweden; Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Erlandsson, Ann
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Environmental and Life Sciences/Biology, Karlstad University, Karlstad, Sweden; Department of Urology, Örebro University Hospital, Örebro, Sweden.
    Effect of macrophages on breast cancer cell proliferation, and on expression of hormone receptors, uPAR and HER-22017Ingår i: International Journal of Oncology, ISSN 1019-6439, Vol. 51, nr 1, s. 104-114Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Malignant tumors, including breast cancers, are frequently infiltrated with innate immune cells and tumor-associated macrophages (TAMs) represent the major inflammatory component in stroma of many tumors. In this study, we examined the immunoreactivity of the macrophage markers CD68 and CD163 as well as the hormone receptors estrogen receptor alpha (ER alpha), progesterone receptor (PR), estrogen receptor beta 1 (ER beta 1), human epidermal growth factor receptor 2 (HER-2), matrix metalloproteinase 9 (MMP-9), urokinase-type plasminogen activator receptor (uPAR) and the proliferations marker Ki67 in 17 breast cancer biopsies. The quantitative score for CD68(+) and CD163(+) strongly indicate M2 phenotype dominance in the currently investigated biopsies. We found that an increasing level of macrophages was negatively associated with ER alpha or PR, whereas a positive association was observed for Ki-67 or uPAR. No significant association could be seen between the level of macrophage and HER-2, ER beta 1 or MMP-9 expression. Effect of conditioned media (CM) generated from cultured human M1 and M2 macrophage phenotypes were investigated on the proliferation and expression of selected markers in the T47D breast cancer cell line. We found that in contrast to the in vivo situation, in particularly the CM from M1 macrophages decreased the growth and Ki67 expression in T47D, and significantly increased ER beta 1 mRNA levels. Moreover, in accordance to the in vivo situation the CM from the macrophages decreased the expression of ER alpha protein as well as ER alpha or PR mRNA. In conclusion our results show that macrophages alone have the capability to decrease the tumor cell expression of ER alpha and PR in vitro. In the tumor environment in vivo macrophages also contribute to an increase in tumor cell expression of uPAR and Ki67, suggesting that macrophages are involved in impairing the prognosis for breast cancer patients.

  • 9.
    Logadottir, Yr
    et al.
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Fall, Magnus
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Gjertsson, Inger
    Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Jirholt, Pernilla
    Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Lindholm, Catharina
    Department of Rheumatology and Inflammation Research, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Peeker, Ralph
    Department of Urology, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Cytokine Expression in Patients with Bladder Pain Syndrome/Interstitial Cystitis ESSIC Type 3C2014Ingår i: Journal of Urology, ISSN 0022-5347, E-ISSN 1527-3792, Vol. 192, nr 5, s. 1564-1568Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: Bladder wall nitric oxide production in patients with bladder pain syndrome type 3C is increased compared to undetectable nitric oxide in patients with nonHunner bladder pain syndrome and healthy controls. However, the underlying mechanism/s of the increased nitric oxide production is largely unknown. We compared mRNA expression of a select group of cytokines in patients with bladder pain syndrome/interstitial cystitis type 3C and in pain-free controls.

    Materials and Methods: Cold cup biopsies from 7 patients with bladder pain syndrome type 3C and 6 healthy subjects were analyzed. mRNA expression of IL-4, 6, 10 and 17A, iNOS, TNF-alpha, TGF-beta and IFN-gamma was estimated by real-time polymerase chain reaction. IL-17 protein expression was determined by immunohistochemistry. Mast cells were labeled with tryptase to evaluate cell appearance and count.

    Results: IL-6, 10 and 17A, and iNOS mRNA levels as well as the number of mast cells infiltrating the bladder mucosa were significantly increased in patients with bladder pain syndrome type 3C compared to healthy controls. TNF-alpha, TGF-beta and IFN-gamma mRNA levels were similar in patients and controls. IL-17A expression at the protein level was up-regulated and localized to inflammatory cells and urothelium in patients with bladder pain syndrome type 3C.

    Conclusions: Patients with bladder pain syndrome/interstitial cystitis had increased mRNA levels of IL-17A, 10 and 6, and iNOS. IL-17A might be important in the inflammatory process. To our knowledge the increase in IL-17A is a novel finding that may have new treatment implications.

  • 10.
    Logadottir, Yr
    et al.
    Department of Urology, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för läkarutbildning.
    Lindholm, Catharina
    Department of Rheumatology and Inflammation Research, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Fall, Magnus
    Sahlgrenska University Hospital, Gothenburg, Sweden.
    Peeker, Ralph
    Department of Urology, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Inflammation characteristics in bladder pain syndrome ESSIC type 3C/classic interstitial cystitis2014Ingår i: International journal of urology, ISSN 0919-8172, E-ISSN 1442-2042, Vol. 21, nr Suppl. 1, s. 75-78Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objectives: Interstitial cystitis is regarded as a heterogenous syndrome with two distinguishable forms: the non-ulcer and the classic form of interstitial cystitis, the latter with Hunner's lesions; or bladder pain syndrome type 3C and non-Hunner bladder pain syndrome, respectively.

    Methods: A cohort of 379 patients diagnosed with interstitial cystitis was studied. Nitric oxide release from the bladder was measured using a chemiluminescence nitric oxide analyzer. Bladder biopsies from the patients and healthy controls were analyzed by routine histopathological examination. Biopsies from a subset of patients and controls were also analyzed by immunohistochemistry and cytokine gene expression by real-time polymerase chain reaction.

    Results: Patients with bladder pain syndrome type 3C/classic interstitial cystitis had considerably higher levels of nitric oxide as compared with non-Hunner bladder pain syndrome/non-ulcer interstitial cystitis patients and healthy individuals, and showed histologically a chronic inflammation in the bladder mucosa, with abundant mast cell infiltration in all layers of the bladder wall. No inflammation was noted in non-Hunner bladder pain syndrome/non-ulcer interstitial cystitis patients. The isoenzymes inducible nitric oxide synthase, the catalyst in the nitric oxide production, was strongly expressed in the inflammatory cells in the bladder mucosa of bladder pain syndrome type 3C/classic interstitial cystitis patients. In addition, the expression of the pro-inflammatory cytokines interleukin-6 and interleukin-17A messenger ribonucleic acid, and of anti-inflammatory interleukin-10 messenger ribonucleic acid showed significantly increased levels in bladder pain syndrome type 3C/classic interstitial cystitis compared with healthy controls.

    Conclusion: Bladder pain syndrome type 3C/classic interstitial cystitis is a distinct inflammatory disease and in many aspects shares features of inflammatory autoimmune diseases. These findings could open up novel research avenues with expectations for new targets for pharmacological treatment.

  • 11.
    Logadottir, Yr
    et al.
    Dept Urol, Inst Clin Sci, Sahlgrenska Acad, University of Gothenburg, Gothenburg, Sweden.
    Hallsberg, Lena
    Dept Surg, Sahlgrenska Acad, Inst Clin Sci, University of Gothenburg, Gothenburg, Sweden.
    Fall, Magnus
    Dept Urol, Sahlgrenska Acad, Inst Clin Sci, University of Gothenburg, Gothenburg, Sweden.
    Peeker, Ralph
    Dept Urol, Sahlgrenska Acad, Inst Clin Sci, University of Gothenburg, Gothenburg, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Bladder pain syndrome/interstitial cystitis ESSIC type 3C: High expression of inducible nitric oxide synthase in inflammatory cells2013Ingår i: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 47, nr 1, s. 52-56Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective. Bladder pain syndrome/interstitial cystitis (BPS/IC) includes a heterogeneous collection of underlying pathological conditions. Compared to the classic IC with a Hunner lesion, now denominated ESSIC type 3C, the non-Hunner type of BPS/IC appears different in a number of respects. In a previous study, measuring luminal nitric oxide (NO) in the bladder of patients with BPS/IC, it was reported that all patients with ESSIC type 3C had high levels of NO. The aim of the present study was to investigate the source of inducible nitric oxide synthase (iNOS) and thereby the cellular origin of NO production via iNOS. Material and methods. Immunohistochemistry, with two different anti-iNOS antibodies, was used to study10 patients with BPS/IC ESSIC type 3C who expressed high levels of intraluminal NO. These results were compared with four patients with non-Hunner BPS/IC. To substantiate further the involvement of iNOS in this condition, the protein expression of nitrotyrosine, a marker for iNOS activation, was also assessed. Results. On routine histopathology, the tissues of type 3C patients exhibited inflammatory infiltrates of varying intensity. Strong immunoreactivity for both iNOS and nitrotyrosine was noted within the urothelium but also within the inflammatory infiltrates in the lamina propria of these subjects. Conclusions. The findings of a clearly detectable protein expression of iNOS in both the urothelium and the inflammatory infiltrates in bladder biopsies from patients with BPS/IC ESSIC type 3C suggest that the production of NO, in this entity, may occur in different tissue compartments.

  • 12.
    Logadottir, Yr
    et al.
    Dept. of Urology, Institute of Clinical Sciences, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.
    Lindholm, Catharina
    Dept. of Rheumatology, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.
    Jirholt, Pernilla
    Dept. of Rheumatology, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.
    Gjertsson, Inger
    Dept. of Rheumatology, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.
    Fall, Magnus
    Dept. of Urology, Institute of Clinical Sciences, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Peeker, Ralph
    Dept. of Urology, Institute of Clinical Sciences, The Sahlgrenska Academy, The University of Gothenburg, Gothenburg, Sweden.
    Cytokine responses in BPS/IC Type 3C2014Ingår i: International journal of urology, ISSN 0919-8172, E-ISSN 1442-2042, Vol. 21, nr Suppl.1, s. A23-A23Artikel i tidskrift (Refereegranskat)
  • 13.
    Mohlin, Camilla
    et al.
    Department of Chemistry and Biomedicine, Linnaeus University, Kalmar, Sweden.
    Delbro, Dick
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Kvanta, Anders
    Department of Clinical Neuroscience, Section for Ophthalmology and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden.
    Johansson, Kjell
    Department of Science, Kristianstad University, Kristianstad, Sweden.
    Evaluation of Congo Red Staining in Degenerating Porcine Photoreceptors In Vitro: Protective Effects by Structural and Trophic Support2018Ingår i: Journal of Histochemistry and Cytochemistry, ISSN 0022-1554, E-ISSN 1551-5044, Vol. 66, nr 9, s. 631-641Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Congo red (CR) is a histological stain used for the detection of extracellular amyloids mediating various neurodegenerative diseases. Given that damaged photoreceptors appear to degenerate similarly to other nerve cells, CR staining was evaluated in experimentally injured porcine retina. CR staining appeared mostly as discrete cytosolic deposits with no obvious plaque formation during the investigated time period. Increases of CR labeling coincided temporally with the known accumulation of mislocalized opsins and increases of cell death. Coculture, either with human retinal pigment epithelium (ARPE) or human neural progenitor (ReN) cells, was accompanied by a significant reduction of CR labeling. Of particular interest was the reduction of CR labeling in cone photoreceptors, which are important for the perception of color and fine details and afflicted in age-related macular degeneration (AMD). Electron microscopy revealed inclusions in the inner segment, cell body, and occasionally synaptic terminals of photoreceptor cells in cultured specimens. Closer examinations indicated the presence of different types of inclusions resembling protein aggregates as well as inclusion bodies. The current results indicate that injury-related response resulted in accumulation of CR deposits in photoreceptor cells, and that trophic and/or structural support attenuated this response.

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