Destruction Of Parenchyma Research Articles

Pyonephrosis drained by double-J catheter.

An infectious disease with obstructive hydronephrosis, pyonephrosis causes suppurative destruction of the renal parenchyma. In such cases, retrograde ureteric stenting is considered a good choice for the drainage of pyonephrosis, as an alternative to percutaneous nephrostomy and nephrectomy. The complication rate is minimal in retrograde ureteric stenting compared with about 4% in percutaneous nephrostomy.

Correlation in Size of Right Lobe and Caudate Lobe of Liver in Normal and Chronic Liver Disease Patients' By Using Ultrasonography

Chronic liver disease in the clinical aspect is a disorder process of the liver. It involves the changes of continuous destruction and regeneration of the liver parenchyma progressing to fibrosis and cirrhosis.

A Study of Chronic Liver Disease by Focusing Cardiovascular Changes

Cirrhotic cardiomyopathy can be explained as chronic dysfunction of the heart exhibited as blunted response to contractile function of the heart during Strain and decreased diastolic rest with odd electrophysiological (QT interval prolongation) adjustments, all taking region within the absence of an present cardiac disorder and irrespective of the reason of cirrhosis. Chronic Liver Disease is a process of revolutionary destruction and regeneration of the liver parenchyma leading to extensive spectrum of changes like persistent hepatitis, cirrhosis or hepatocellular carcinoma. Cirrhosis is one of the maximum common presentation of persistent liver sicknesses. It is characterized with the aid of reduced contractile responsiveness to stress, altered diastolic relaxation and electrophysiological abnormalities (QT interval prolongation) all happening within the absence of existing cardiac sickness. At gift there is evidence that, compromised liver feature and portal high blood pressure with splanchnic vasodilatation lead to the improvement of the hyperdynamic adjustments. Also other elements like increased sympathetic pastime, accelerated blood go with the flow and presence of arteriovenous communications can play extensive role in pathogenesis. Many pathophysiological mechanisms like decreased beta-receptor motion seem to be involved within the cardiac and autonomic disorder. Cirrhotic cardiomyopathy may be proven through tissue Doppler imaging and it's far quality tested with the aid of pharmacological or bodily strain. Diagnosis is done through 2D echocardiography, electrocardiography and cardiac serum markers (Troponin I, NT pro BNP). Elevation of troponin I is accepted to be a marker of cirrhotic cardiomyopathy. Troponin I proves to be a significant marker of myocardial injury in chronic liver disease patients. Although NT pro BNP is elevated as it can be elevated in fluid overload state related to liver disease it is unlikely to take it significant. The cardiovascular changes in the present study indicates that there was myocardial characterised by elevated troponin I.

The MMP-2/TIMP-2 System in Alzheimer Disease.

Alzheimer Disease (AD) is the most prevalent type of dementia. Pathological changes in the AD brain include Amyloid β-protein (Aβ) plaques and Neurofibrillary Tangles (NFTs), as well as extensive neuronal and synaptic loss. Matrix Metalloproteinase-2 (MMP-2) is a neutral, zinc-dependent protease that primarily targets extracellular matrix proteins. MMP-2 activity is strictly controlled, and its dysregulation has been implicated in a variety of pathologies, including AD. In this brief review, we discussed the contributions of dysregulated MMP-2 activity and an imbalanced interaction between MMP-2 and its endogenous inhibitor, Tissue Inhibitors of Metalloproteinase-2 (TIMP-2), to AD. We also described the underlying mechanisms of the effects of MMP-2/TIMP-2, both beneficial and detrimental, on AD, including: (1) MMP-2 directly degrades Aβ resulting in the clearance of Aβ deposits. Conversely, Aβ-induced MMP-2 may contribute to brain parenchymal destruction. (2) MMP-2 induces breakdown of BBB, and this deleterious effect could be reversed by TIMP-2. (3) MMP-2 disrupts oxidative homeostasis in AD. (4) MMP-2 has both proinflammatory/pro-angiogenetic and antiinflammatory/ anti-angiogenetic effects on AD. Besides, we discuss the clinical utility of MMP- 2/TIMP-2 as therapeutic targets for AD.

Extracorporeal Shock Waves Increase Markers of Cellular Proliferation in Bronchial Epithelium and in Primary Bronchial Fibroblasts of COPD Patients.

Chronic obstructive pulmonary disease (COPD) is due to structural changes and narrowing of small airways and parenchymal destruction (loss of the alveolar attachment as a result of pulmonary emphysema), which all lead to airflow limitation. Extracorporeal shock waves (ESW) increase cell proliferation and differentiation of connective tissue fibroblasts. To date no studies are available on ESW treatment of human bronchial fibroblasts and epithelial cells from COPD and control subjects. We obtained primary bronchial fibroblasts from bronchial biopsies of 3 patients with mild/moderate COPD and 3 control smokers with normal lung function. 16HBE cells were also studied. Cells were treated with a piezoelectric shock wave generator at low energy (0.3 mJ/mm2, 500 pulses). After treatment, viability was evaluated and cells were recultured and followed up for 4, 24, 48, and 72 h. Cell growth (WST-1 test) was assessed, and proliferation markers were analyzed by qRT-PCR in cell lysates and by ELISA tests in cell supernatants and cell lysates. After ESW treatment, we observed a significant increase of cell proliferation in all cell types. C-Kit (CD117) mRNA was significantly increased in 16HBE cells at 4 h. Protein levels were significantly increased for c-Kit (CD117) at 4 h in 16HBE (p < 0.0001) and at 24 h in COPD-fibroblasts (p = 0.037); for PCNA at 4 h in 16HBE (p = 0.046); for Thy1 (CD90) at 24 and 72 h in CS-fibroblasts (p = 0.031 and p = 0.041); for TGFβ1 at 72 h in CS-fibroblasts (p = 0.038); for procollagen-1 at 4 h in COPD-fibroblasts (p = 0.020); and for NF-κB-p65 at 4 and 24 h in 16HBE (p = 0.015 and p = 0.0002). In the peripheral lung tissue of a representative COPD patient, alveolar type II epithelial cells (TTF‐1+) coexpressing c-Kit (CD117) and PCNA were occasionally observed. These data show an increase of cell proliferation induced by a low dosage of extracorporeal shock waves in 16HBE cells and primary bronchial fibroblasts of COPD and control smoking subjects.

Renal Replacement Lipomatosis Presenting as Hematuria

Renal replacement lipomatosis (RRL) is an extremely rare condition. It is thought to be a spectrum of degenerative process classically characterized by extensive abundance of adipose tissue in kidney. RRL is associated with long standing inflammation and stone disease in 70% of cases. In severe cases, it may lead to complete parenchymal destruction. Rarely, RRL may mimic fatty neoplasm of kidney. We report a 62-year-old male with renal replacement lipomatosis associated with stone disease presenting as hematuria.

Emerging Roles of Long Non-Coding RNAs in Renal Fibrosis.

Renal fibrosis is an unavoidable consequence that occurs in nearly all of the nephropathies. It is characterized by a superabundant deposition and accumulation of extracellular matrix (ECM). All compartments in the kidney can be affected, including interstitium, glomeruli, vasculature, and other connective tissue, during the pathogenesis of renal fibrosis. The development of this process eventually causes destruction of renal parenchyma and end-stage renal failure, which is a devastating disease that requires renal replacement therapies. Recently, long non-coding RNAs (lncRNAs) have been emerging as key regulators governing gene expression and affecting various biological processes. These versatile roles include transcriptional regulation, organization of nuclear domains, and the regulation of RNA molecules or proteins. Current evidence proposes the involvement of lncRNAs in the pathologic process of kidney fibrosis. In this review, the biological relevance of lncRNAs in renal fibrosis will be clarified as important novel regulators and potential therapeutic targets. The biology, and subsequently the current understanding, of lncRNAs in renal fibrosis are demonstrated—highlighting the involvement of lncRNAs in kidney cell function, phenotype transition, and vascular damage and rarefaction. Finally, we discuss challenges and future prospects of lncRNAs in diagnostic markers and potential therapeutic targets, hoping to further inspire the management of renal fibrosis.

Novel Respiratory Disability Score Predicts COPD Exacerbations and Mortality in the SPIROMICS Cohort.

RationaleSome COPD patients develop extreme breathlessness, decreased exercise capacity and poor health status yet respiratory disability is poorly characterized as a distinct phenotype.ObjectiveTo define respiratory disability in COPD based on available functional measures and to determine associations with risk for exacerbations and death.MethodsWe analyzed baseline data from a multi-center observational study (SPIROMICS). This analysis includes 2332 participants (472 with severe COPD, 991 with mild/moderate COPD, 726 smokers without airflow obstruction and 143 non-smoking controls).MeasurementsWe defined respiratory disability by ≥4 of 7 criteria: mMRC dyspnea scale ≥3; Veterans Specific Activity Questionnaire <5; 6-minute walking distance <250 m; St George’s Respiratory Questionnaire activity domain >60; COPD Assessment Test >20; fatigue (FACIT-F Trial Outcome Index) <50; SF-12 <20.ResultsUsing these criteria, respiratory disability was identified in 315 (13.5%) participants (52.1% female). Frequencies were severe COPD 34.5%; mild-moderate COPD 11.2%; smokers without obstruction 5.2% and never-smokers 2.1%. Compared with others, participants with disability had more emphysema (13.2 vs. 6.6%) and air-trapping (37.0 vs. 21.6%) on HRCT (P<0.0001). Using principal components analysis to derive a disability score, two factors explained 71% of variance, and a cut point −1.0 reliably identified disability. This disability score independently predicted future exacerbations (ß=0.34; CI 0.12, 0.64; P=0.003) and death (HR 2.97; CI 1.54, 5.75; P=0.001). Thus, participants with disability by this criterion had almost three times greater mortality compared to those without disability.ConclusionOur novel SPIROMICS respiratory disability score in COPD was associated with worse airflow obstruction as well as airway wall thickening, lung parenchymal destruction and certain inflammatory biomarkers. The disability score also proved to be an independent predictor of future exacerbations and death. These findings validate disability as an important phenotype in the spectrum of COPD.

Impact of diet and genes on murine autoimmune pancreatitis.

The impact of environmental factors, such as diet, and the genetic basis of autoimmune pancreatitis (AIP) are largely unknown. Here, we used an experimental murine AIP model to identify the contribution of diet to AIP development, as well as to fine‐map AIP‐associated genes in outbred mice prone to develop the disease. For this purpose, we fed mice of an autoimmune‐prone intercross line (AIL) three different diets (control, calorie‐reduced and western diet) for 6 months, at which point the mice were genotyped and phenotyped for AIP. Overall, 269 out of 734 mice (36.6%) developed AIP with signs of parenchymal destruction, equally affecting mice of both sexes. AIP prevalence and severity were reduced by approximately 50% in mice held under caloric restriction compared to those fed control or western diet. We identified a quantitative trait locus (QTL) on chromosome 4 to be associated with AIP, which is located within a previously reported QTL. This association does not change when considering diet or sex as an additional variable for the mapping. Using whole‐genome sequences of the AIL founder strains, we resolved this QTL to a single candidate gene, namely Map3k7. Expression of Map3k7 was largely restricted to islet cells as well as lymphocytes found in the exocrine pancreas of mice with AIP. Our studies suggest a major impact of diet on AIP. Furthermore, we identify Map3k7 as a novel susceptibility gene for experimental AIP. Both findings warrant clinical translation.

A clinicopathological study of Xanthogranulomatous pyelonephritis

Introduction: Rare, severe and atypical form of chronic pyelonephritis characterized by destruction of renal parenchyma and the presence of granulomas, abscesses, and collection of lipid filled macrophages. Objective: To study the clinicopathological relationship of the lesion. Method: A 8 year retrospective study was done to analyze the lesions of renal and ureteric calculi. XGP was found to be most common in female. Conclusion: Xanthogranulomatous pyelonephritis is unusual variant of chronic pyelonephritis. Preoperative diagnosis is desirable with laboratory analysis. Histopathological examination is important to know the type and etiological factor of the lesion.

Role of Exocrine and Endocrine Insufficiency in the Management of Patients with Chronic Pancreatitis.

Background: Exocrine pancreatic insufficiency results from the destruction of the pancreatic parenchyma and is diagnosed by using direct or indirect tests, both of which have shortcomings. Chronic pancreatitis is the most frequent cause of this pathology in adults. Methods: Patients meeting radiological or histological diagnostic criteria of chronic pancreatitis are enrolled and the stool elastase test is conducted, considering fecal elastase levels >200 µg/g to represent normal pancreatic function, and levels <200 μg/g to indicate the presence of exocrine pancreatic insufficiency. Additionally, we determine the body mass index of the patients and study their nutritional status and main biochemical and hematological variables, including their glucose and hemoglobin A1c (HbA1c) levels. Results: Exocrine pancreatic insufficiency is detected in 60% of the patients. Among these, 83.3% are severe cases, and 72% of the latter also are diagnosed with endocrine pancreatic insufficiency (diabetes mellitus). During the nutritional status study, HbA1c levels are significantly higher, and magnesium and prealbumin levels are significantly lower in patients with exocrine pancreatic insufficiency than in those without this disease. Conclusions: Exocrine and endocrine pancreatic insufficiency are highly prevalent among patients with chronic pancreatitis and an early diagnosis of these diseases is vital to improve the clinical management of these patients and reduce their risk of mortality.

Tuberculosis testicular: presentación de un caso y revisión de la literatura

Descripción del caso clínico: Presentamos el caso de un paciente masculino de 33 años con historia familiar de tuberculosis pulmonar, quien acude a consulta por presentar fiebre de predominio nocturno y percepción de masa testicular derecha no dolorosa, sin otro síntoma asociado, marcadores tumorales en rangos normales.&#x0D; Relevancia: De acuerdo con cifras de la OMS (Organización Mundial de la Salud), la infección por Mycobacterium tuberculosis es considerada la infección oportunista más frecuente en el mundo.&#x0D; Conclusión: La presentación clínica característica de la tuberculosis testicular (TbT) es una masa testicular no dolorosa, difícil de diferenciar de una tumoración maligna. Los hallazgos inespecíficos en los exámenes de laboratorio e imagen acompañados de baja sospecha diagnóstica llevan a un alto porcentaje de diagnósticos tardíos. Hoy en día una cantidad considerable de pacientes se detectan por hallazgos de patología en la pieza quirúrgica. Si bien el pronóstico a corto y mediano plazo suele ser favorable, una de las complicaciones a largo plazo de la TbT es la infertilidad secundaria a la destrucción del parénquima testicular y/o la obstrucción del trayecto de salida de los espermatozoides.

Study the Cytochrome P450 Gene Expression Changes in Iraqi Patients with Chronic Liver Disease

The cytochrome P450 is a chemical group of heme-containing proteins speaks to one of the biggest and most practically various superfamilies’ found in nature. Chronic liver disease (CLD) is a the process of the liver that involves a process of progressive destruction and regeneration of the liver parenchyma leading to fibrosis and cirrhosis. The aim of this study to assessment the cytochrome P450 gene expression changes of three variants, CYP1A2, CYP2B6, and CYP2E1 in Iraqi patients with chronic liver disease(hepatitis+ alcoholism and hepatitis+ non-alcoholism).CYP1A2, CYP2B6, and CYP2E1 mRNA gene expression were assessed by quantitative real time PCR (qRT-PCR) in 50 cases with CLD and 50 subjects as control. Primers for genes of interest, CYP1A2, CYP2B6, and CYP2E1mRNA and housekeeping gene (GAPDH) were designed by using NCBI tools. Fatty acid synthase (FAS) was estimated by ELISA technique. The results showing statically significant differences in FAS levels (ng/ml) between study groups, HC, HNC, and control (p-value&lt; 0.05). GEF in CYP1A2 gene showing no change between HC and control but there were statistical variations in GEF in HNC and both HC or control. GEF in CYP2B6 and CYP2E1 genes showing highly significant differences between control and both HNC and HC. In conclusion, CYP2B6 and CYP2E1 gene expression were risk factor for progression HC but not HNC through stimulation of increasing levels of FAS.

The relationship between quantitative computed tomography parameters and spirometry measures of disease severity in chronic obstructive pulmonary disease

Background: Chronic obstructive pulmonary disease (COPD) is characterized by emphysematous destruction of lung parenchyma and airway remodeling which lead to limitation of airflow. Computed tomography is of considerable value in quantifying the severity of the disease in COPD either by visual or by quantitative CT techniques (QCT). This study was designed to assess the relationship between quantitative computed tomography parameters and spirometric measurements of disease severity in cases with COPD. Materials and Methods: A total of 100 cases between age group 41 to 65 years, who were proved to have COPD by pulmonary function test were recruited. Inspiratory CT was designed to take a deep breath and plain CT chest was taken at full inspiration to obtain total lung capacity. Expiratory CT was asked to hold breath in normal expiration and CT chest was taken to obtain functional residual capacity. Inner and outer diameters and wall thick ness were measured manually and their average value was considered. Correlations analysis was conducted between spirometric measurements and QCT measures. Results: The mean values of low attenuation areas in inspiration

Role of yttrium-90 selective internal radiation therapy in the treatment of liver-dominant metastatic colorectal cancer: an evidence-based expert consensus algorithm.

Surgical resection of colorectal liver metastases is associated with greater survival compared with non-surgical treatment, and a meaningful possibility of cure. However, the majority of patients are not eligible for resection and may require other non-surgical interventions, such as liver-directed therapies, to be converted to surgical eligibility. Given the number of available therapies, a general framework is needed that outlines the specific roles of chemotherapy, surgery, and locoregional treatments [including selective internal radiation therapy (SIRT) with Y-90 microspheres]. Using a data-driven, modified Delphi process, an expert panel of surgical oncologists, transplant surgeons, and hepatopancreatobiliary (HPB) surgeons convened to create a comprehensive, evidence-based treatment algorithm that includes appropriate treatment options for patients stratified by their eligibility for surgical treatment. The group coined a novel, more inclusive phrase for targeted locoregional tumor treatment (a blanket term for resection, ablation, and other emerging locoregional treatments): local parenchymal tumor destruction therapy. The expert panel proposed new nomenclature for 3 distinct disease categories of liver-dominant metastatic colorectal cancer that is consistent with other tumor types: (I) surgically treatable (resectable); (II) surgically untreatable (borderline resectable); (III) advanced surgically untreatable (unresectable) disease. Patients may present at any point in the algorithm and move between categories depending on their response to therapy. The broad intent of therapy is to transition patients toward individualized treatments where possible, given the survival advantage that resection offers in the context of a comprehensive treatment plan. This article reviews what is known about the role of SIRT with Y-90 as neoadjuvant, definitive, or palliative therapy in these different clinical situations and provides insight into when treatment with SIRT with Y-90 may be appropriate and useful, organized into distinct treatment algorithm steps.

Optimum imaging of chronic pancreatitis.

Chronic pancreatitis is an inflammatory process of the pancreas characterized by progressive parenchyma destruction, resulting in pain and exocrine and endocrine insufficiency. In the advanced stages the diagnosis by imaging is usually straightforward, while in the early phases of the disease there can be a paucity of findings at imaging, thus making an early diagnosis challenging. Different imaging modalities can have a role in the initial diagnosis and in the longitudinal follow-up of patients affected by chronic pancreatitis, also enabling to assess the complications of the disease. Radiography, Ultrasonography, CT and MRI can all provide morphological information, and MRI with the administration of secretin can also provide functional information. The use of an appropriate technique is fundamental for optimizing the examination to the clinical question.

Computed tomography in the diagnosis of exogenous allergic alveolitis from the exposure of industrial aerosols

Developed CTVR- criteria for the destruction of the pulmonary parenchyma in patients with exogenous allergic alveolitis from the exposure of various industrial aerosols to reveal the peculiarities of formation and course of disease. 2 groups (203 patients) with alveolitis of different etiology were examined. Comparative analysis of the results of the study showed the importance of CTVR in the diagnosis of professional alveolitis.

An Open-label Study With Pirfenidone on Chronic Hypersensitivity Pneumonitis

BackgroundChronic hypersensitivity pneumonitis (cHP) represents a severe lung disease often evolving to fibrosis with the subsequent destruction of the lung parenchyma. There are no approved therapies with confirmed efficacy to deal with this disease. MethodsWe performed an open-label, proof of concept study, to evaluate the efficacy and safety of pirfenidone added to immunosuppressive drugs on the treatment of cHP. We included 22 patients assigned to two groups: Group 1, nine patients that received prednisone plus azathioprine and Group 2, thirteen patients, received prednisone plus azathioprine and pirfenidone (ClinicalTrials.gov identifier NCT02496182). There were no significant imbalances in clinically relevant baseline characteristics between two study groups. ResultsAfter 1 year of treatment, inclusion of pirfenidone was not associated with improved forced vital capacity (primary end-point). A not significant tendency to show higher improvement of diffusion capacity of the lung for carbon monoxide (DLCO) was observed in the group receiving pirfenidone (p=0.06). Likewise, a significant improvement in the total score on the SGRQ was found in the group 2 (p=0.02) without differences in other two questionnaires related to quality of life (ATAQ-IPF and EQ-5D-3L). HRCT showed a decrease of the ground glass attenuation without changes in the fibrotic lesions and without differences between both groups. ConclusionsThese findings suggest that the addition of pirfenidone to the anti-inflammatory treatment in patients with chronic HP may improve the outcome with acceptable safety profile. However, prospective randomized double-blind, placebo-controlled trials in largest cohorts are needed to validate its efficacy.

Urological infections in the developing world: an increasing problem in developed countries.

Infectious diseases that often follow geographical distribution patterns are increasingly crossing such boundaries, aided by human travel and commerce. These pose a new challenge to physicians who are required to diagnose previously unseen conditions and address drug-resistant organisms. We review some such common infections. A literature review was performed for six common urological infections and a narrative review based on recent publications on these infections was compiled. In Urology, some infections that are now crossing geographical boundaries include Brucellosis, Schistosomiasis, Tuberculosis, Filariasis, Hydatidosis and emphysematous pyelonephritis. Brucellosis, a zoonotic infection, is common in the Mediterranean areas, Asia, South America and Africa. Infection can involve all parts of the genitourinary tract. Schistosomiasis, a parasitic disease, is particularly common in Sub-Saharan Africa and may have bacterial superinfection. Voiding symptoms are common and bladder carcinoma may develop. Tuberculosis affects almost every organ in the body and in the male genital system, often presents with abscesses, nodules, ulcers and infertility that is difficult to manage. Filariasis is caused by two species of worms and is transmitted through a bite from a mosquito carrying larvae of the worm. It causes lymphatic obstruction leading to scrotal edema, hydrocoele to elephantiasis of scrotum. Emphysematous pyelonephritis is a life-threatening suppurative necrotizing infection of the renal parenchyma. While not being geographically limited, it is more common in developing areas with poor health care access. Genitourinary hydatidosis is a rare disease that is associated mainly with renal involvement in the genitourinary tract. Large cysts with destruction of renal parenchyma may be found. Although uncommon, these urological infections are associated with significant morbidity and mortality and awareness in all healthcare settings is now an essential requirement.

LJ-2698, an Adenosine A3 Receptor Antagonist, Alleviates Elastase-Induced Pulmonary Emphysema in Mice.

Emphysema, a major component of chronic obstructive pulmonary disease (COPD), is a leading cause of human death worldwide. The progressive deterioration of lung function that occurs in the disease is caused by chronic inflammation of the airway and destruction of the lung parenchyma. Despite the main impact of inflammation on the pathogenesis of emphysema, current therapeutic regimens mainly offer symptomatic relief and preservation of lung function with little therapeutic impact. In the present study, we aimed to discover novel therapeutics that suppress the pathogenesis of emphysema. Here, we show that LJ-2698, a novel and highly selective antagonist of the adenosine A3 receptor, a G protein-coupled receptor involved in various inflammatory diseases, significantly reversed the elastase-induced destructive changes in murine lungs. We found that LJ-2698 significantly prevented elastase-induced airspace enlargement, resulting in restoration of pulmonary function without causing any obvious changes in body weight in mice. LJ-2698 was found to inhibit matrix metalloproteinase activity and pulmonary cell apoptosis in the murine lung. LJ-2698 treatment induced increases in anti-inflammatory cytokines in macrophages at doses that displayed no significant cytotoxicity in normal cell lines derived from various organs. Treatment with LJ-2698 significantly increased the number of anti-inflammatory M2 macrophages in the lungs. These results implicate the adenosine A3 receptor in the pathogenesis of emphysema. Our findings also demonstrate the potential of LJ-2698 as a novel therapeutic/preventive agent in suppressing disease development with limited toxicity.