Bladder Damage Research Articles

Open Reduction With Internal Fixation in Locked Pubic Symphysis: A Case Presentation

Regarding the fact that lateral compression is usually not the underlying mechanism of fracture, Locked pubic symphysis is a very rare injury. At most times it can be managed with closed reduction method; however, open reduction with or without internal fixation may sometimes be required. In rare cases, osteotomy is the only choice. Urethral or bladder damage can occasionally be found. In this study, we presented a case of locked pubic symphysis with failed closed reduction who underwent successful open reduction with internal fixation.

Liposomal formulations of oxybutynin and resiniferatoxin for the treatment of urinary diseases: improvement of drug tolerance upon intravesical.

The use of liposomes for drug release has demonstrated to be a promising therapeutic platform for biomedical applications. In this study, intravesical administration of OXI (1.5mM) and RTX (100nM) was used to compare histological changes caused in Wistar female rats by the drugs both unloaded and loaded in liposomes. After instillation of formulations by intravesical catheter, bladders were removed and histological analysis carried out at pre-determined time intervals over a period of 60days. Urinalysis was performed to verify the presence of infection and of liposomes. Results showed that RTX caused a higher bladder damage, with inflammatory reaction that reached all bladder layers. After 60days, RTX-treated group showed urothelial alterations, collagen replacement by fibrosis and also abdominal adherence, but not the OXI-treated group. At the end of the assay, the liposomal-treated groups showed a minimal inflammatory reaction and significantly increased bladder size. Moreover, urinalysis confirmed the presence of liposomes in rat urine. RTX promoted higher bladder damage than OXI. Intravesical administration of liposomal OXI or RTX formulations minimized inflammatory reaction, with an extended drug effect on bladders. After a single intravesical administration, liposomes were found in rat urine samples after 60days.

Extracorporeal Shock Wave Therapy Protected the Functional and Architectural Integrity of Rodent Urinary Bladder against Ketamine-Induced Damage.

This study tested the hypothesis that extracorporeal-shock-wave (ECSW) protected the functional and anatomical integrity of rat urinary-bladder against ketamine-induced damage. In in vitro study, the rat bladder smooth muscle cells (RBdSMCs) were categorized into G1 (sham-control), G2 (RBdSMCs + menadione), G3 (RBdSMCs + ECSW) and G4 (RBdSMCs + menadione + ECSW). The results showed protein expressions of oxidative-stress/mitochondrial-damaged biomarkers (NOX-1/NOX-2/oxidized protein/cytosolic-cytochrome-C/cyclophilin-D), inflammatory markers (MyD88/TRAF6/p-IKB-α/NF-κB/TNF-α/IL-6/IL-1ß/MMP-9/iNOS), and cell-stress response signalings (ASK1/p-MKK4/p-MKK7/ERK1/2//p-JNK/p-p38/p-53) were significantly increased in G2 than in G1 and G3, and those were significantly reversed in G4 (all p < 0.0001). Adult-male SD rats (n = 24) were equally categorized into group 1 (sham-control), group 2 (ketamine/30 mg/kg/daily i.p. injection for four weeks), group 3 [ketamine/30 mg/kg + ECSW/optimal energy (0.12 mJ/mm2/120 impulses/at 3 h and days 3/7/14/21/28 after ketamine administration)] and group 4 [(ketamine/30 mg/kg + ECSW/higher energy (0.16 mJ/mm2/120 impulses)] and animals were euthanized by day 42. The results showed the urine levels of pro-inflammatory cytokines (TNF-α/IL-6) were lowest in group 1, highest in group 2 and significantly higher in group 3 than in group 4 at days 1/7/14/28 (all p < 0.0001). The duration of urinary bladder contraction was lowest in group 2, highest in group 1 and significantly higher in group 4 than in group 3, whereas the maximal pressure of urinary bladder exhibited an opposite pattern of bladder contraction among the groups (all p < 0.0001). The histopathological findings of fibrosis/inflammation/keratinization and protein expressions of oxidative-stress/mitochondrial-damaged biomarkers (NOX-1/NOX-2/oxidized protein/cytosolic-cytochrome-C/cyclophilin-D), and inflammatory (TLR-2/TLR-4/MyD88/TRAF6/p-IKB-α/NF-κB/TNF-α/IL-1ß/MMP-9/iNOS) and cell-stress response (ASK1/p-MKK4/p-MKK7/ERK1/2//p-JNK/p-p38) signalings and apoptotic/fibrotic biomarkers (cleaved-caspas3/cleaved-PARB/Smad3/TFG-ß) exhibited an identical pattern of urine proinflammatory cytokine among the groups (all p < 0.0001). ECSW effectively attenuated ketamine-induced bladder damage and dysfunction.

Pathophysiology and Management of Long-term Complications After Transvaginal Urethral Diverticulectomy.

Female urethral diverticulum (UD) is a rare and benign condition that presents as an epithelium-lined outpouching of the urethra. It has various symptoms, of which incontinence in the form of postmicturition dribble is the most common. The gold standard for the diagnosis of UD is magnetic resonance imaging, and the treatment of choice is transvaginal diverticulectomy. Despite the high success rate of transvaginal diverticulectomy, postoperative complications such as de novo stress urinary incontinence (SUI), recurrence, urethrovaginal fistula, recurrent urinary tract infections, newly-onset urgency, and urethral stricture can occur. De novo SUI is thought to result from weakening of the anatomical support of the urethra and bladder neck or damage to the urethral sphincter mechanism during diverticulectomy. It can be managed conservatively or may require surgical treatment such as a pubovaginal sling, Burch colposuspension, or urethral bulking agent injection. Concomitant SUI can be managed by concurrent or staged anti-incontinence surgery. Recurrent UD may be a newly formed diverticulum or the result of a remnant diverticulum from the previous diverticulectomy. In cases of recurrent UD requiring surgical repair, placing a rectus fascia pubovaginal sling may be an effective method to improve the surgical outcome. Urethrovaginal fistula is a rare, but devastating complication after urethral diverticulectomy; applying a Martius flap during fistula repair may improve the likelihood of a successful result. Malignancies in UD are rarely reported, and anterior pelvic exenteration is the recommended management in such cases.

Long-term ketamine administration induces bladder damage and upregulates autophagy-associated proteins in bladder smooth muscle tissue.

Long-term ketamine abuse can cause significant lower urinary tract symptoms in humans, termed ketamine-associated cystitis (KC). Here, we established a model of long-term (6 months) ketamine administration in wild-type (C57BL/6) mice. We elucidated the pathological effects of ketamine in the bladder and investigated changes in autophagy-associated protein expression (i.e., LC3, Beclin-1, and P62) and inflammatory cytokines (i.e., IL-6 and IL-1β) in the bladder smooth muscle tissue. Long-term ketamine administration reduced the number of layers in the bladder mucosal epithelial cells (4-5 layers in the saline group vs. 2-3 layers in the ketamine groups), but increased the number of mast cells and collagen fibers. LC3-II/LC3-I, Beclin-1, IL-6, and IL-1β protein expression in the bladder smooth muscle tissues of ketamine-treated mice was significantly increased. The mRNA and protein levels of P62 in the Ket-60 mg/kg group were also significantly increased, but not the Ket-30 mg/kg group. Our results reveal that long-term ketamine administration can cause cystitis-like pathological changes in mice, and the disordered autophagy in the bladder tissue may be involved in the persistent bladder damage following long-term administration of ketamine at 60 mg/kg.

Double benefit of metformin treatment: improved bladder function in cyclophosphamide-induced cystitis and enhanced cytotoxicity in cancer cells

Cyclophosphamide (CP) is a widely used anti-neoplastic drug; however, it leads to bladder dysfunction in the form of hemorrhagic cystitis that is a serious dose-limiting complication in cancer patients. We aimed to evaluate the protective effects of metformin (MET) in a mouse model of CP-related cystitis in parallel with its effect on CP-induced cytotoxicity in a breast cancer cell line, MDA-MB-231. Cystitis was induced by a single intraperitoneal injection of CP (300 mg/kg), and mice were administered MET, mesna, or vehicle treatment. 24 hours after cystitis induction, the bladders were removed for histopathological analysis and ex vivo evaluation of detrusor muscle contractility. The effect of MET on the cytotoxicity of CP in MDA-MB-231 cells was evaluated as the viability of the cells via MTT assay. Histopathological evaluation confirmed that CP induced a severe cystitis, and MET partially inhibited CP-induced bladder damage. Carbachol-evoked cholinergic contractions were significantly decreased in detrusor strips of mice injected with CP only compared to control (Emax=293.67± 20.00 vs. 497.79± 21.78 mg tension/mg tissue, respectively). In CP-injected mice, treatment with 100 mg/kg MET restored cholinergic contractions (Emax=473.72±62.61 mg tension/mg tissue). In MDA-MB-231 cells, MET decreased their viability, and the combination of MET and CP caused more decrease in cell viability as compared to CP alone (p<0.05), demonstrating that MET enhances the cytotoxicity of CP in these cancer cells. Our results indicate that MET has a strong potential as a therapeutic adjuvant to prevent CP-induced cystitis while enhancing the efficacy of CP.

Bladder injury – A team challenge

"Abstract: Bladder trauma is caused by a direct blow to the distended bladder, severe injury fracturing the pelvis, iatrogenic, or penetrating wounds. Early detection and diagnosis are key to successful management of cases, but omission or late reveal of bladder damage increase mortality and create long-term problems. A bladder injury may not always present with immediate obvious signs and symptoms, especially in a multi-trauma patient, who is also more difficult to investigate. Moreover, during the COVID-19 pandemic, delayed patients’ access to tertiary, multidisciplinary hospitals, increases the risk for delayed diagnosis and also increases the need for more specialists from different surgical and non-surgical areas to raise their awareness of less common manifestations of bladder trauma. We present a review of literature and cases of less common bladder damage from the perspective of a multi-disciplinary team in the University Emergency Hospital in Bucharest. Keywords: bladder injury, pelvic fracture, urinary fistula"

Bladder damage in locally advanced colorectal cancer

Bladder damage in locally advanced colorectal cancer

Toksičnost radioterapije kod pacijenata sa karcinomom prostate

Prostate cancer (PC) is the most frequent male tumor, accounting for about one-third of all cancers in men. Since survival is often favorable regardless of therapy, treatment decisions may depend on therapy-specific health outcomes. The majority of men initially diagnosed with localized PC ultimately die with, rather than of, their disease. As a result, men who are diagnosed will live many years with the treatment's sequelae. The major therapeutic strategies include radical prostatectomy or external beam radiotherapy. Radiotherapy is one of the curative treatment options. The tumor dose-response relationship has been studied and is widely accepted. The unsatisfactory local control with doses &lt; 70 Gy led to dose escalation using highly precise radiotherapy techniques - three-dimensional conformal radiotherapy and intensity-modulated radiotherapy enabling the delivery of high radiation doses up to 74 - 78 Gy. Bowel, rectal and urinary toxicities are the principal limiting factors in delivering a high dose. Acute symptoms include a change in bowel habits, urgency, and fecal incontinence. The most commonly reported late toxicities were chronic diarrhea, proctitis, or rectal bleeding. Several factors have been associated with increased gastrointestinal toxicity such as larger bowel volume receiving high doses, the patient's age, diabetes, and concomitant use of androgen deprivation therapy. Bladder damage resulting from acute radiation toxicity is manifested as radiation cystitis (frequent urination and dysuric disorders). Smoking, previous abdominopelvic surgeries and the use of diuretics significantly affect the occurrence of acute genitourinary toxicity grade ≥ 2. Risk factors for the development of late genitourinary complications are higher radiation dose, previous urinary problems, transurethral interventions, and acute genitourinary complications. It is essential to strike a balance between the therapeutic benefits and radiotherapy side effects. Severe late complications significantly reduce the quality of life (QOL) of PC survivors. Early detection and proper evaluation of complications are especially important in increasing the patient's QOL.

Bovine tunica albuginea conserved in honey as xenograft for cystoplasty in rats

ABSTRACT: Urinary bladder damages leading to few viable bladder tissue available might demand a challenging reconstructive surgery. In this context, biomaterials are valid alternatives for bladder reconstruction. This study evaluated the bovine tunica albuginea fragment as graft material for cystoplasty in rats and honey-preserved implant viability.Thirty Wistar rats were assigned to two groups: (1) a test group (T) with a circular 1.0-cm-diameterbovine tunica albuginea graft application in the apex region by a continuous absorbable (Polyglactin 910 5-0) suture with stitching of all bladder layers and (2) a simulation group (S) in which animals underwent only partial cystectomy. In addition, each of these groups was further divided into three subgroups according to euthanasia period on post-surgery day 7, 15 and 30.Two animals had self-limiting hematuria at postsurgical period. At necropsy, frequent crystals and adhesion to the peritoneum were observed. At the histopathological evaluation, animals from the T group euthanized by 15th postoperative day had layers disorganization and initial muscle development, while T group rats euthanized by 30th postoperative day showed complete urothelization. Urothelization pattern was similar in both groups. Moreover, the muscular layer formation was present in both groups, but more evident in S group animals. Nevertheless, inflammatory infiltrate and neovascularization were remarkably more intense in T group rats.It might be concluded that bovine tunica albuginea graft was successful in repairing rats’ bladder, being a good biomaterial option in reconstructive urinary vesicle surgery.

Prostate cancer survivors with symptoms of radiation cystitis have elevated fibrotic and vascular proteins in urine.

Radiation for pelvic cancers can result in severe bladder damage and radiation cystitis (RC), which is characterized by chronic inflammation, fibrosis, and vascular damage. RC development is poorly understood because bladder biopsies are difficult to obtain. The goal of this study is to gain understanding of molecular changes that drive radiation-induced cystitis in cancer survivors using urine samples from prostate cancer survivors with history of radiation therapy. 94 urine samples were collected from prostate cancer survivors with (n = 85) and without (n = 9) history of radiation therapy. 15 patients with radiation history were officially diagnosed with radiation cystitis. Levels of 47 different proteins were measured using Multiplex Luminex. Comparisons were made between non-irradiated and irradiated samples, and within irradiated samples based on radiation cystitis diagnosis, symptom scores or hematuria. Statistical analysis was performed using Welch's t-test. In prostate cancer survivors with history of radiation therapy, elevated levels of PAI 1, TIMP1, TIMP2, HGF and VEGF-A were detected in patients that received a radiation cystitis diagnosis. These proteins were also increased in patients suffering from hematuria or high symptom scores. No inflammatory proteins were detected in the urine, except in patients with gross hematuria and end stage radiation cystitis. Active fibrosis and vascular distress is detectable in the urine through elevated levels of associated proteins. Inflammation is only detected in urine of patients with end-stage radiation cystitis disease. These results suggest that fibrosis and vascular damage drive the development of radiation cystitis and could lead to the development of more targeted treatments.

Transurethral resection of a bladder trigone leiomyoma: a rare case report

BackgroundBladder leiomyomas are rare and benign tumors of the bladder. They account for 0.43% of all bladder tumors, and only 250 cases have been reported in English literature. Based on the size and localization of the lesion, their symptoms vary considerably. Women seem to be more affected, and obstructive symptoms predominate. Surgical treatment is almost always highly effective, leaving a low recurrence rate.Case presentationWe present a clinical case of a 52-year old man with macroscopic hematuria and obstructive lower urinary tract symptoms due to a large bladder trigone leiomyoma. CT and MRI showed a well-defined large bladder leiomyoma and cystoscopy established the initial findings. The patient underwent successful transurethral resection of the lesion, and pathology findings confirmed the diagnosis.ConclusionsThis case report demonstrates that transurethral resection of a large bladder trigone leiomyoma is a feasible and successful procedure. Long term follow-up proves that there is neither scarring distortion of the bladder trigone area nor damage in the ureteral orifices, even though there was a thorough removal of the trigone wall.

Regulation of Cellular Stress Signaling in Bladder Ischemia.

IntroductionThe etiology of lower urinary tract symptoms in patients with non-obstructed non-neurogenic bladder remains largely unknown. Clinical studies divulged a significant correlation between reduced bladder blood flow and low bladder compliance. Animal models of bladder ischemia displayed structural modifications, characterized by loss of smooth muscle cells and accumulation of connective tissue in the bladder wall. The underlying mechanisms contributing to structural damage in bladder ischemia remain largely elusive. We previously reported that structural modifications in bladder ischemia correlate with upregulated stress proteins and cell survival signaling, suggesting the potential role of cellular stress in ischemic damage. However, stress response molecules and downstream pathways eliciting bladder damage in ischemia remain largely undetermined.MethodsUsing a rat model of bladder ischemia along with a cell culture hypoxia model, we investigated stress signaling molecules in the ischemic bladder tissues and hypoxic bladder smooth muscle cells.ResultsOur data suggest simultaneous upregulation of two major cellular stress-sensing molecules, namely apoptosis signal-regulating kinase 1 (ASK1) and caspase-3, implying degenerative insult via stress signaling pathway in bladder ischemia. Consistent with bladder ischemia, incubation of cultured human bladder smooth muscle cells at low oxygen tension increased both ASK1 and caspase-3 expression, insinuating hypoxia as an essential factor in ASK1 and caspase-3 upregulation. Gene deletion of ASK1 by ASK1 siRNA in cultured smooth muscle cells prevented caspase-3 upregulation by hypoxia, suggesting caspase-3 regulation by ASK1 under the ischemic/hypoxic conditions. Upregulation of ASK1 and caspase-3 in rat bladder ischemia and human bladder smooth muscle cell hypoxia was associated with subcellular structural modifications consistent with the initial stages of apoptotic insult.ConclusionOur data suggest that stress sensing by ASK1 and caspase-3 may contribute to subcellular structural damage and low bladder compliance. The ASK1/caspase-3 pathway may provide therapeutic targets against cellular stress and degenerative responses in bladder ischemia.

Are we repeating mistakes of the past? A review of the evidence for esketamine.

Esketamine has been licensed for 'treatment-resistant depression' in the USA, UK and Europe. Licensing trials did not establish efficacy: two trials were negative, one showed a statistically significant but clinically uncertain effect, and a flawed discontinuation trial was included, against Food and Drug Administration precedent. Safety signals - deaths, including suicides, and bladder damage - were minimised.

Abstract IA11: Bladder cancers affecting transplant recipients harbor diverse viruses that associate with overall survival

Abstract BK polyomavirus (BKPyV) is a ubiquitous virus that establishes a lifelong subclinical infection in the urinary tract. In transplant recipients, BKPyV can reactivate and cause kidney and bladder damage. Recent sequencing studies of tumors from transplant recipients have revealed that BKPyV sequences are present in approximately 25% of bladder tumors. This is dramatically higher than the &amp;lt;1% rate of BKPyV detection observed in muscle-invasive bladder cancers affecting the general population. Like cancer-causing human papillomaviruses (HPVs), BKPyV has been shown to upregulate the human cytosine deaminase APOBEC3B, which has emerged as the second most abundant source of point mutations in human cancers. Furthermore, the APOBEC3-associated mutation signature is the most abundant mutational signature in bladder cancer. To comprehensively assess the role of BKPyV and other viruses in bladder cancer from solid organ transplant recipients, we used a database linking US transplant and cancer registries to identify and collect 44 archived primary bladder tumors, 5 metastases, and 15 adjacent normal tissue specimens. Whole-genome and total RNA sequencing was performed on the samples. From these data, we detected BKPyV in 18% of primary tumors. In five cases, there is clear evidence of BKPyV integration into the host cell genome, and all cases show transcription of the viral tumor antigens. In a separate set of analyses, BKPyV transcription was detected in 3.7% of non-muscle-invasive early-stage bladder cancer cases affecting the general population. Our surveys also detected other viruses, including high- and low-risk HPVs, JC polyomavirus (JCPyV), and anelloviruses, at lower frequencies. Two primary-metastatic pairs maintained clonally integrated HPV or BKPyV and respective viral oncogene expression in the metastatic lesions. Nearly all tumors had dominant APOBEC3 signature mutations, and BKPyV-positive tumors expressed significantly more APOBEC3B compared to virus-negative tumors or normal tissues. Tumors from four kidney transplant patients showed high mutation burden consistent with exposure to aristolochic acid, a nephrotoxic carcinogen found in some herbal supplements. Clinical data indicate that BKPyV-positive tumors are predominantly high grade with invasive behavior. Strikingly, survival was significantly shorter for patients whose tumors harbored BKPyV or JCPyV (9.7 and 8.4 months, respectively) compared to patients with tumors harboring HPV or no detectable viruses (65.8 and 50.2 months, respectively). This study comprehensively characterizes the genomes and transcriptomes of tumors, revealing several distinct tumor etiologies that impact patient outcome. Citation Format: Gabriel J. Starrett, Kelly Yu, David Petersen, Petra Lenz, Lars Dyrskjøt, Paul Meltzer, Eric Engels, Christopher B. Buck. Bladder cancers affecting transplant recipients harbor diverse viruses that associate with overall survival [abstract]. In: Proceedings of the AACR Special Conference on the Microbiome, Viruses, and Cancer; 2020 Feb 21-24; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2020;80(8 Suppl):Abstract nr IA11.

Are oxidative stress and ischemia significant causes of bladder damage leading to lower urinary tract dysfunction? Report from the ICI-RS 2019.

Several studies indicate that pelvic ischemia and oxidative stress may play a significant role in lower urinary tract dysfunction (LUTD), including detrusor overactivity (DO)/overactive bladder (OAB) and detrusor underactivity (DU)/underactive bladder (UAB). The present article addresses proposal 1: "Are oxidative stress and ischemia significant causes of bladder damage leading to LUTD?" from the 2019 International Consultation on Incontinence-Research Society (ICI-RS) meeting. Bladder ischemia in animals and humans is briefly described, along with the proposed progression from ischemia to LUTD. Bladder ischemia is compared with ischemia of other organs, and the ongoing development of pelvic ischemia animal models is discussed. In addition, the distribution of blood within the bladder during filling and voiding and the challenges of quantification of blood flow in vivo are described. Furthermore, oxidative stress, including potential biomarkers and treatments, and challenges regarding antioxidant therapy for the treatment of LUTD are discussed. Finally, seven critical research questions and proposed studies to answer those questions were identified as priorities that would lead to major advances in the understanding and treatment of lower urinary tract symptoms (LUTS)/LUTD associated with pelvic ischemia and oxidative stress.

Cigarette smoke induces the pyroptosis of urothelial cells through ROS/NLRP3/caspase-1 signaling pathway.

Cell death and inflammation are involved in the development of bladder dysfunction. Pyroptosis is programmed cell death, causing cytotoxic effects and local inflammation. As one of the biggest health threats in the world, smoking is also closely related to urinary system diseases. The aims of this study were to investigate the role of NLRP3 inflammasome-mediated pyroptosis in the bladder after cigarette smoke exposure. The expression of NLRP3 inflammasome and the activity of caspase-1 in bladder tissue was investigated after cigarette smoke exposure. In vitro, bladder urothelial cells were stimulated by cigarette smoke extract and then the activity of caspase-1 and the expression of NLRP3 inflammasome were measured. The role of oxidative stress was also assessed. The activity of caspase-1 in bladder tissue increased by 50% after cigarette smoke exposure. Cigarette smoke caused oxidative stress injury and the activation of NLRP3 inflammasome. In addition, reactive oxygen species (ROS) inhibitor N-acetyl-cysteine alleviated the pyroptosis of urothelial cells. Cigarette smoke-induced pyroptosis of bladder tissue by activating ROS/NLRP3/caspase-1 signaling pathway. Inhibition of bladder urothelial cell pyroptosis may be a new approach to alleviate bladder damage caused by smoking.

Role of Doppler ultrasound and Creatine Kinase as a Biochemical Marker in Diagnosis of Placenta Accreta

Placenta accreta is a life-threatening obstetric condition requiring cesarean hysterectomy for management. Placenta accreta was diagnosed by gray-scale ultrasonography, color Doppler imaging, and magnetic resonance imaging. Creatine kinase (CK) is an enzyme expressed by various tissues and cell types. This study compared between creatine kinase as biological marker and ultrasound and Doppler findings for prenatal detection of morbid placentation in anterior placenta on scar of previous cesarean section. The current study is a prospective cohort observational study, Led In Benha educating support doctor's facility on 50 pregnant ladies Hosting placenta accreta coating scar about past uterine surgery. Every one incorporated ladies were conveyed Eventually Tom's perusing caesarian segments for intend gestational agdistis during conveyance might have been 34. 5 ± 2 weeks. Done ladies with low parity, youthful age, or the individuals who wanted to preserve their fertility, preservationist methodology might have been trailed. Cs hysterectomy might have been performed over 28 (90. 32%) ladies. There might have been a noteworthy Acquaintanceship between 2D-GS ultrasonography discoveries Also troublesome placental separation, need for included intraoperative steps, necessity to cs hysterectomy What's more bladder damage with affectability 90% and specificity 60%. CK distinguished 10 patients crazy about 31 with placenta accreta Also 18 patients crazy about 19 without placental invasion, its affectability 30% and specificity. Joining 2DGS with CK test demonstrated huge change to auc worth about CK. 2D grayscale U/S required a great screening ability for those prediction of sequele from claiming dismal placentation in ladies for placenta previa. CK it is questionable test alone for antenatal finding from claiming morbidly follower placenta.

Houttuynia cordata Extract Ameliorates Bladder Damage and Improves Bladder Symptoms via Anti-Inflammatory Effect in Rats with Interstitial Cystitis.

The mechanism of interstitial cystitis/bladder pain syndrome (IC/BPS) remains unclear to date, but reports showed that bladder inflammation and increasing number of activating mast cells in bladder tissues were common in patients with IC/BPS. Houttuynia cordata is widely used in Chinese traditional medicine, and its function of anti-inflammation has been proved. The purpose of this study was to investigate the efficacy and possible mechanisms of the Houttuynia cordata (HC) extract in the treatment of interstitial cystitis/bladder pain syndrome (IC/BPS). In the current study, a total of 30 adult female rats were randomly divided into three groups: sham group (n = 10), cyclophosphamide + saline (CYP + NS) group (n = 10), and cyclophosphamide + Houttuynia cordata extract (CYP + HC) group (n = 10). The animal model of IC/BPS was induced with cyclophosphamide (75 mg/kg, intraperitoneal injection, once every 3 days for 10 days) in the CYP + NS group and CYP + HC group, and sham rats received a volume-matched injection of saline. After anesthesia with urethane (0.8 g/kg, intraperitoneal injection), intravesical administration of either saline (1 ml) or Houttuynia cordata extract (1 ml, 2 g/ml) was continued once per day for a week in the CYP + NS group and CYP + HC group, respectively. Subsequently, urinary frequency, nociceptive behaviors, cystometry, bladder weight, histological changes, and cytokine (IL-6, IL-8, TNF-α) concentration were evaluated and compared among the three groups. Variables including inflammatory grade, mast cell number, proportion of activated mast cells, bladder weight, cytokine concentration of bladder homogenates, and frequency of urination significantly increased in the CYP + NS group compared with the sham group (P < 0.01) and CYP + HC group (P < 0.01). Besides, compared with the CYP + NS group, longer intercontraction interval, bigger bladder capacity, higher nociceptive threshold, fewer number of mast cells, and lower proportion of activated mast cells were found in the CYP + HC group (P < 0.01). Our study demonstrated that the Houttuynia cordata extract can effectively inhibit mast cell proliferation and activation and downregulate proinflammatory cytokine in a rat model of IC/BPS induced with cyclophosphamide and might be potentially valuable for the treatment of IC/BPS.

Protective Effects of Boron on Cyclophosphamide-Induced Bladder Damage and Oxidative Stress in Rats.

This study aims to investigate protective effects of boron against cyclophosphamide-induced bladder toxicity that produces oxidative stress and leads to apoptosis of the cells. In total, 24 rats were divided into 4 equal groups. The control group received saline. The 2nd experimental group received 200mgkg of cyclophosphamide i.p. on the 4th day while the 3rd group was given only boron (200mgkg, i.p.) for 6days. In the 4th group, boron was given for 6days and cyclophosphamide (200mgkg, i.p.) was administrated on the 4th day. Twenty-four hours after the last boron or cyclophosphamide administration, rats were sacrificed under anesthesia. Bladder tissues of rats were taken for histological and immunohistochemical (apoptotic markers such as caspase-3, bcl-2, and bax) and blood was taken for the biochemical (serum total thiol, serum natural thiol, serum thiol-disulfide) analysis. Transient epithelial thinning, edema, marked inflammatory reaction, and bleeding were observed in bladders of the group that received cyclophosphamide. Also, the activity of bax and caspase-3-positive cells increased while the number of bcl-2-positive cells decreased. In the same group, serum natural thiol and total thiol levels decreased while serum disulfide levels increased, which indicates oxidative stress. On the other hand, in the boron+cyclophosphamide group pretreatment with boron protected, the bladder tissue and the number of bcl-2-positive cells increased, and bax and caspase-3-positive cells decreased, showing antiapoptotic effects of boron against cyclophosphamide-induced toxicity. In parallel with the findings of this group, native thiol and total thiol levels increased and serum disulfide levels decreased pointing out to a decreased oxidative stress. Our results indicate that boron pretreatment significantly protects rat bladder against cyclophosphamide-induced bladder damage due to its antiapoptotic and antioxidant properties.