scholarly journals Morphological and structural variants of cellular and stromal interaction in a focus of destruction in acute lung abscess and lung gangrene in term of formation and stabilisation of fibrin-associated processes

2008 ◽  
pp. 75-80
Author(s):  
Ya. N. Shoikhet ◽  
A. V. Lepilov ◽  
Yu. G. Motin ◽  
A. P. Bochkarev
Keyword(s):  
Lung Tissue ◽  
Structural Changes ◽  
Lung Parenchyma ◽  
Lung Abscess ◽  
Pathological Examination ◽  
Cell Reaction ◽  
Acute Lung Inflammation ◽  
Anatomic Structure ◽  
Bilateral Lung ◽  
Tissue Specimens

Purulent and destructive lung diseases are often complicated by loss of anatomic structure of lung tissue, development of lung cirrhosis with subsequent respiratory and heart failure. We performed pathomorphological examination of operational and post mortem lung tissue specimens from 116 inpatients of 25 to 78 years of age with acute lung abscess or lung gangrene who was treated at a pulmonology center from 1999 to 2005. Acute lung inflammation tending to suppuration was characterized by pronounced cell reaction with no "fibrin blockage" and resulted in extended histolysis and abscess formation. "Young" fibrin was often found. Microvessels were fully passable, full-blooded with no fibrin into lumen. At subacute stage, fibrin was "maturing" with subsequent organization and growth of granulated tissue. Clinically, there were sequestered lung abscesses. Massive deposits of "young" and "maturing" fibrin formed "fibrin cocoon" with macrophages and neutrophils bricked up inside. Cell reaction was weak. There were swelling and desquamation of endothelium of microvessels, massive fibrin deposits into vessel lumen and prominent perivascular impregnation with fibrin. This pathological variant could lead to formation of abscess or pulmonary fibrosis with carnification. In cases of massive subtotal or total, often bilateral lung injury with weak delimiting of purulent and destructive process massive destructive zones with resting lung parenchyma faintly impregnated with fibrin were seen. There were no features of fibrin deposition inside microvessels. Functional activity of neutrophils and macrophages was greatly decreased. Therefore, the most favourable pathohistological variant appears to be formation of fibrin blockage consisted of "young" fibrin deposits; prominent cell reaction and absence of microcirculatory block. Structural changes of cells and stroma should be considered during pathological examination in order to provide optimal treatment strategy.

scholarly journals Some pathogenic aspects of pulmonary emphysema in COPD patients

2008 ◽  
pp. 48-53
Author(s):  
A. V. Averyanov ◽  
M. V. Samsonova ◽  
A. L. Chernyaev ◽  
A. G. Chuchalin ◽  
A. E. Polivanova ◽  
...  
Keyword(s):  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Lung Tissue ◽  
Transforming Growth Factor ◽  
Interstitial Fibrosis ◽  
Lung Parenchyma ◽  
Vascular Wall ◽  
Transforming Growth Factor Β1 ◽  
Compensatory Mechanisms ◽  
Tissue Specimens

Histological and immunohistochemical investigations of lung tissue specimens were performed in 9 patients with COPD underwent lung volume reduction surgery. Lung tissue specimens of died persons without lung and heart pathology were as controls. Tissue expressions of endothelial growth factor (EGF), type 9 matrix metalloproteinase, type 1 matrix metalloproteinase (TIMP-1) tissue inhibitor, and transforming growth factor β1 (TGF β-1) have been studied. Patents with severe emphysema typically had focal interstitial fibrosis, interalveolar septa infiltrated with interstitial macrophages and lymphocytes, hypertrophy of media and proliferation of intima in the vascular wall, and arteriolar muscularization. There was significantly higher expression of EGF and TIMM-1 in the lung tissue of these patients compared with controls; this could confirm the presence of compensatory mechanisms of lung parenchyma destruction. Strong correlations were found between expression of EGF and TGF β-1, EGF and TIMP-1 which demonstrated a relationship between angiogenesis, proteolysis and fibrogenesis in development of emphysema.

Suppression of cell proliferation and programmed cell death by dexamethasone during postnatal lung development

2002 ◽  
Vol 282 (3) ◽  
pp. L477-L483 ◽  
Author(s):  
Cédric Luyet ◽  
Peter H. Burri ◽  
Johannes C. Schittny
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Lung Development ◽  
Structural Changes ◽  
Tissue Transglutaminase ◽  
Lung Parenchyma ◽  
Lung Maturation ◽  
Morphological Criteria ◽  
Postnatal Lung Development

Prematurely born babies are often treated with glucocorticoids. We studied the consequences of an early postnatal and short dexamethasone treatment (0.1–0.01 μg/g, days 1–4) on lung development in rats, focusing on its influence on peaks of cell proliferation around day 4 and of programmed cell death at days 19–21. By morphological criteria, we observed a dexamethasone-induced premature maturation of the septa ( day 4), followed by a transient septal immatureness and delayed alveolarization leading to complete rescue of the structural changes. The numbers of proliferating (anti-Ki67) and dying cells (TdT-mediated dUTP nick end labeling) were determined and compared with controls. In dexamethasone-treated animals, both the peak of cell proliferation and the peak of programmed cell death were reduced to baseline, whereas the expression of tissue transglutaminase (transglutaminase-C), another marker for postnatal lung maturation, was not significantly altered. We hypothesize that a short neonatal course of dexamethasone leads to severe but transient structural changes of the lung parenchyma and influences the balance between cell proliferation and cell death even in later stages of lung maturation.

scholarly journals Abstract P-32: Lung Structural Changes in Covid-19 Patients

2021 ◽  
Vol 11 (Suppl_1) ◽  
pp. S25-S26
Author(s):  
Valeriy Kartashev ◽  
Djamshid Mardonov ◽  
Bahshillo Mamirov ◽  
Azamat Butaev
Keyword(s):  
Lung Tissue ◽  
Structural Changes ◽  
Ground Glass ◽  
Parietal Pleura ◽  
Lesion Volume ◽  
Autopsy Material ◽  
Severe Condition ◽  
Inflammatory Infiltration ◽  
Subsequent Transformation ◽  
Primary Diagnostics

Background: The main causes of death from Covid-19 are lung lesions with the development of respiratory failure. However, structural changes in the lung tissue in this pathology are poorly studied. We examined autopsy material from patients with Covid-19. The severe condition of patients, the manifestation of pulmonary symptoms of damage (cough, dyspnea) and the high probability of viral pneumonia at COVID-19 led to the widespread use of CT diagnostics in this group of patients, which allowed to identify of the primary signs of the disease, their subsequent transformation as well as the most adverse radiation symptoms corresponding to the severe course of the process (Speranskaya, 2020; Pan et al., 2019). In the cases studied by us, the detection of typical symptoms revealed by radiation diagnostics of COVID-19 was subsequently confirmed by PCR data, which may indicate a high information content and specificity of detecting CT symptoms of a lesion as a method of primary diagnostics. The aim of our study is to confirm at the microscopic level the correspondence of MSCT changes. Methods: The material was taken at autopsy of deceased patients, fixed in 10% formalin solution in phosphate buffer, paraffin sections were stained with hematoxylin and eosin. The autopsy material was examined using a Carl Zeiss light microscope, Axioskop 40. Results: Studies have shown that most of the alveoli of the lung tissue kept their airiness. However, their lumens were significantly reduced due to a significant thickening of the interalveolar septa caused by pronounced inflammatory infiltration mainly by lymphocytes. The most significant changes were revealed from the side of the microvasculature. There are numerous blood clots of various sizes in the lumen of most micro-vessels. The walls of microvessels have been significantly thickened with pronounced inflammatory infiltration and significant edema. The lumens of microvessels have been characterized by significant polymorphism. Intraluminal clots have been also characterized by pronounced polymorphism. The parietal pleura has been thickened. This has been reflected in the MSCT images and corresponds to the processes of perivascular infiltration. Conclusion: The primary CT pattern of COVID-19 is a picture of infiltration of individual secondary pulmonary lobules of the "ground glass" type, followed by a decrease in the lesion volume at a favorable course of the disease, or their increase, the addition of a CT picture of a "cobblestone pavement" and the appearance of alveolar infiltration in the area of "ground glass" at the unfavorable course of the disease.

scholarly journals SURGICAL ASPECTS OF DIAGNOSIS AND TREATMENT OF CHEST PATHOLOGY CAUSED BY CORONAVIRUS DISEASE COVID-19, ANALYSIS OF CLINICAL CASE

2020 ◽  
Vol 19 (4) ◽  
pp. 25-31
Author(s):  
V. Yatskyv ◽  
B. Maksymyuk ◽  
S. Frimet ◽  
Ya. Hyrla ◽  
S. Mereuca
Keyword(s):  
Personal Experience ◽  
Viral Infections ◽  
Specific Treatment ◽  
Lung Parenchyma ◽  
Surgical Interventions ◽  
Medical Institutions ◽  
Surgical Tactics ◽  
Bilateral Lung ◽  
Surgical Aspects ◽  
Basic Medical

The COVID-19 pandemic has generated many challenges both for humanity in general, and for the systems of organizing medical care and many areas of specialized treatment, in particular surgical. The very dynamics of the pandemic, the lack of available specific treatment, various approaches to assessing statistical and clinical data in various countries today do not allow generally accepted conclusions to be drawn. Numerous publications on this topic, as a rule, contain information about personal experience of research, diagnosis, treatment and a review of the current literature. We analyzed 68 cases of chest diseases caused by COVID-19 in patients who received consultative, specialized surgical thoracic care in basic medical institutions of Chernivtsi region for the period January-September 2020. Bilateral lung lesions predominated – 70.6 % in older patients 42 years (66.2 %). Surgical interventions were performed in 65 (95.6 %) patients. The most common complication in the acute period was pneumothorax on the background of active viral pneumonia – 40 (58.8 %) patients, 6 (8.8 %) – patients with heart and pericardial lesions, 7 (10.3 %) – hemorrhagic, serous-fibrinous pleurisy. Based on own data in comparison with the histological and pathophysiological researches resulted in the available literature, surgical tactics, separate surgical receptions at patients with virus-induced complications, in particular: drainage of a pleural cavity, pericardium, videothoracoscopic techniques are proved. The algorithm of examinations and treatment tactics in the formation of intrapulmonary pseudocysts after coronavirus disease are presented. We analyzed 5 (7.4 %) cases in which there were complications of major diseases (cancer, nonspecific purulent-septic diseases) caused by COVID-19. Study of the effectiveness of the use of videothoracoscopic electric welding technologies in the destruction of the lung parenchyma caused by viral infections.

scholarly journals Clinico-physiological profile of patients of pulmonary impairment after tuberculosis at a tertiary care centre

2018 ◽  
Vol 6 (9) ◽  
pp. 2999
Author(s):  
Gajendra V. Singh ◽  
Antriksh Srivastava ◽  
Vinisha Chandra ◽  
Santosh Kumar ◽  
Rishabh Goel
Keyword(s):  
Pulmonary Tuberculosis ◽  
Exercise Tolerance ◽  
Structural Changes ◽  
Tertiary Care ◽  
Uttar Pradesh ◽  
Lung Parenchyma ◽  
Tertiary Care Centre ◽  
Physiological Profile ◽  
Pulmonary Impairment

Background: Pulmonary tuberculosis (TB) is a unique infectious disease that more often results in permanent structural changes in the lung parenchyma. It is by virtue of these changes that the patients even after bacteriological cure continue to suffer the after effects of the disease. Objective of study was to assess the clinico-physiological profile of patients of pulmonary impairment after tuberculosis (PIAT) attending S. N. Medical College, Agra, Uttar Pradesh, India.Methods: Over the time period of 2 years, 350 patients of healed pulmonary tuberculosis were identified and studied about their clinico-physiological profile. This profile included age, sex, category of treatment, pulmonary function test pattern, exercising capacity, exercise tolerance and quality of life.Results: It was found that majority of the patients were males, >60 years of age and had taken Category-II treatment. Most of the patients were having an obstructive pattern on PFT, poor exercise tolerance and exercise capacity and a poor quality of life.Conclusions: Patients of healed pulmonary TB continue to experience respiratory symptoms owing to the permanent anatomical changes in the lung conferred by the disease.

The release of slow-reacting substance of anaphylaxis from guinea pig lung: effects of calcium antagonists

1985 ◽  
Vol 63 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Melissa A. Damiano ◽  
Edward J. Barbieri
Keyword(s):  
Guinea Pig ◽  
Intracellular Calcium ◽  
Lung Tissue ◽  
Calcium Antagonists ◽  
Lung Parenchyma ◽  
Free Medium ◽  
Bicarbonate Buffer ◽  
Normal Medium ◽  
Voltage Dependent ◽  
High Concentrations

The effects of three calcium antagonists, verapamil, lanthanum, and 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) were studied on the release of slow-reacting substance of anaphylaxis (SRS-A) from ovalbumin-sensitized chopped guinea pig lung parenchyma in calcium-containing and calcium-free media. The SRS-A levels (mean ± SEM) obtained from tissues incubated in normal and calcium-free Krebs–bicarbonate buffer were 51 ± 8 (N = 19) and 21 ± 4 (N = 14) U/mL, respectively. TMB-8 (0.1–10 μM) a reported intracellular calcium antagonist, reduced antigen-stimulated SRS-A release from lung tissue incubated in calcium-containing, but not calcium-free, medium; A23187-induced SRS-A release from normal guinea pig lung was not significantly altered by TMB-8 at concentrations up to 10 μM. Verapamil and lanthanum consistently reduced SRS-A release only at high concentrations (100 μM and 1 mM, respectively). The quantities of SRS-A released from lung tissue incubated in the presence of verapamil in normal medium were similar to those obtained in calcium-free medium. Tissues incubated in the presence of potassium chloride (60 and 100 mM) did not release significant quantities of SRS-A, and release which did occur was not blocked by verapamil, suggesting that antigen-induced SRS-A release is not dependent on membrane depolarization and that verapamil was not exerting inhibition via blockade of voltage-dependent calcium channels. These data suggest that although intracellular calcium is important for the regulation of SRS-A secretion from guinea pig lung tissue, extracellular calcium is necessary for optimal release of SRS-A.

A STUDY OF RESIDUAL BREAST TISSUE IN POST MASTECTOMY SKIN FLAP

2021 ◽  
pp. 7-9
Author(s):  
Rubal Gangopadhyay ◽  
Mala Mistri ◽  
Sukanta Sikdar
Keyword(s):  
Breast Carcinoma ◽  
Chest Wall ◽  
Breast Tissue ◽  
Skin Flap ◽  
Carcinogenic Risk ◽  
Pathological Examination ◽  
Cancer Tissue ◽  
Medical College ◽  
Tissue Specimens ◽  
A Prospective Study

Background: The objective of any mastectomy is to rid the chest wall of any breast tissue but since the breast being unencapsulated, there is every chance that some amount of breast tissue may be left behind in the skin aps after resection. As the remnant breast tissue is likely to be exposed to the same carcinogenic risk factors as the tissue removed. Hence, there is always a possibility that the residual tissue may become the seat of a recurrence. To get rid the chest wall so far the residual breast tissue will Objective: be minimal and the recurrence of breast carcinoma will be less. Patents Data source: of proven case of CA breast who underwent MRM at RG KAR MEDICAL COLLEGE AND HOSPITAL from July 2016 to June 2018 are included in the study group. This is a prospective study Study design: of total 45 patients are selected. Materials and methods: Prospective analysis of 45 post MRM women whose mean age is 49.5 years (mean ± SD age, 49.5 ± 2.4 years). Tissue specimens taken from central part of four quadrants of two skin aps for histo-pathological examination. Skin ap thickness measured for more than 8mm. All patients followed for any recurrence of breast carcinoma. Results: Of all histo-pathological specimens left sided breast cancer cases were more common than right side. 48-49 years age group had the most number of cases and more than 53 years the least. The lower medial quadrant the most 5(45.45%), upper and lower lateral quadrant 3(27.27%) each for positive and upper medial quadrant negative for breast tissue. Breast carcinoma negative in all specimens. Skin ap necrosis of 2(4.44%) cases. No recurrences noted during my study period. My study has demonstrated presence of residual breast tis Conclusion: sue in a signicant percentage of post mastectomy skin aps. No residual cancer tissue was found. During the duration of the study, no recurrence of breast carcinoma was detected in patients with residual breast tissue in skin aps.

scholarly journals Cigarette smoke alters the transcriptome of non-involved lung tissue in lung adenocarcinoma patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Giulia Pintarelli ◽  
Sara Noci ◽  
Davide Maspero ◽  
Angela Pettinicchio ◽  
Matteo Dugo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Adenocarcinoma ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Gene Networks ◽  
Lung Parenchyma ◽  
Fold Change ◽  
Differentially Expressed ◽  
Significant Gene ◽  
Never Smokers

Abstract Alterations in the gene expression of organs in contact with the environment may signal exposure to toxins. To identify genes in lung tissue whose expression levels are altered by cigarette smoking, we compared the transcriptomes of lung tissue between 118 ever smokers and 58 never smokers. In all cases, the tissue studied was non-involved lung tissue obtained at lobectomy from patients with lung adenocarcinoma. Of the 17,097 genes analyzed, 357 were differentially expressed between ever smokers and never smokers (FDR < 0.05), including 290 genes that were up-regulated and 67 down-regulated in ever smokers. For 85 genes, the absolute value of the fold change was ≥2. The gene with the smallest FDR was MYO1A (FDR = 6.9 × 10−4) while the gene with the largest difference between groups was FGG (fold change = 31.60). Overall, 100 of the genes identified in this study (38.6%) had previously been found to associate with smoking in at least one of four previously reported datasets of non-involved lung tissue. Seven genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) were differentially expressed between ever and never smokers in all five datasets, with concordant higher expression in ever smokers. Smoking-induced up-regulation of six of these genes was also observed in a transcription dataset from lung tissue of non-cancer patients. Among the three most significant gene networks, two are involved in immunity and inflammation and one in cell death. Overall, this study shows that the lung parenchyma transcriptome of smokers has altered gene expression and that these alterations are reproducible in different series of smokers across countries. Moreover, this study identified a seven-gene panel that reflects lung tissue exposure to cigarette smoke.

scholarly journals Effective lung-targeted RNAi in mice with peptide-based delivery of nucleic acid

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kaido Kurrikoff ◽  
Krista Freimann ◽  
Kadi-Liis Veiman ◽  
Elin Madli Peets ◽  
Andres Piirsoo ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Nucleic Acid ◽  
Lung Disease ◽  
Lung Tissue ◽  
Lung Inflammation ◽  
Disease Models ◽  
Nucleic Acid Delivery ◽  
Acute Lung Inflammation ◽  
Disease Symptoms ◽  
Targeted Gene Therapy

AbstractWe have previously developed efficient peptide-based nucleic acid delivery vectors PF14 and NF55, where we have shown that these vectors preferentially transfect lung tissue upon systemic administration with the nucleic acid. In the current work, we have explored the utilization and potential of these vectors for the lung-targeted gene therapy. Accordingly, we assessed the efficacy of these peptides in (i) two different lung disease models – acute lung inflammation and asthma in mice and (ii) using two different nucleic acid cargos – siRNA and pDNA encoding shRNA. Using RNAi against cytokine TNFα, we showed efficient anti-inflammatory effects in both disease models and observed decreased disease symptoms. Our results highlight the potential of our transfection vectors for lung gene therapy.

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