The importance of antivirus in surgery

1938 ◽  
Vol 34 (1) ◽  
pp. 108-108
Author(s):  
B. Ivanov

Antivirus is used in surgery, firstly, to treat infected wounds and inflammatory processes of the skin and mucous membranes, and, secondly, to prevent and treat inflammatory diseases of the peritoneum and abdominal cavity.

2019 ◽  
Vol 20 (3) ◽  
pp. 459 ◽  
Author(s):  
Leila Kheirandish-Gozal ◽  
David Gozal

Obstructive sleep apnea syndrome (OSAS) is a markedly prevalent condition across the lifespan, particularly in overweight and obese individuals, which has been associated with an independent risk for neurocognitive, behavioral, and mood problems as well as cardiovascular and metabolic morbidities, ultimately fostering increases in overall mortality rates. In adult patients, excessive daytime sleepiness (EDS) is the most frequent symptom leading to clinical referral for evaluation and treatment, but classic EDS features are less likely to be reported in children, particularly among those with normal body-mass index. The cumulative evidence collected over the last two decades supports a conceptual framework, whereby sleep-disordered breathing in general and more particularly OSAS should be viewed as low-grade chronic inflammatory diseases. Accordingly, it is assumed that a proportion of the morbid phenotypic signature in OSAS is causally explained by underlying inflammatory processes inducing end-organ dysfunction. Here, the published links between OSAS and systemic inflammation will be critically reviewed, with special focus on the pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), since these constitute classical prototypes of the large spectrum of inflammatory molecules that have been explored in OSAS patients.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wen-Teng Chang ◽  
Ming-Yuan Hong ◽  
Chien-Liang Chen ◽  
Chi-Yuan Hwang ◽  
Cheng-Chieh Tsai ◽  
...  

Abstract Background Glucocorticoids (GCs) have been extensively used as essential modulators in clinical infectious and inflammatory diseases. The GC receptor (GR) is a transcription factor belonging to the nuclear receptor family that regulates anti-inflammatory processes and releases pro-inflammatory cytokines, such as interleukin (IL)-6. Results Five putative GR binding sites and other transcriptional factor binding sites were identified on theIL-6 promoter, and dexamethasone (DEX) was noted to reduce the lipopolysaccharide (LPS)-induced IL-6 production. Among mutant transcriptional factor binding sites, nuclear factor-kappa B (NF-κB), activator protein (AP)-1, and specificity protein (Sp)1–2 sites reduced basal and LPS-induced IL-6 promoter activities through various responses. The second GR binding site (GR2) was noted to play a crucial role in both basal and inducible promoter activities in LPS-induced inflammation. Conclusions We concluded that selective GR2 modulator might exert agonistic and antagonistic effects and could activate crucial signaling pathways during the LPS-stimulated inflammatory process.


1995 ◽  
Vol 4 (1) ◽  
pp. 5-15 ◽  
Author(s):  
C. Haanen ◽  
I. Vermes

During the last few decades it has been recognized that cell death is not the consequence of accidental injury, but is the expression of a cell suicide programme. Kerr et al. (1972) introduced the term apoptosis. This form of cell death is under the influence of hormones, growth factors and cytokines, which depending upon the receptors present on the target cells, may activate a genetically controlled cell elimination process. During apoptosis the cell membrane remains intact and the cell breaks into apoptotic bodies, which are phagocytosed. Apoptosis, in contrast to necrosis, is not harmful to the host and does not induce any inflammatory reaction. The principal event that leads to inflammatory disease is cell damage, induced by chemical/physical injury, anoxia or starvation. Cell damage means leakage of cell contents into the adjacent tissues, resulting in the capillary transmigration of granulocytes to the injured tissue. The accumulation of neutrophils and release of enzymes and oxygen radicals enhances the inflammatory reaction. Until now there has been little research into the factors controlling the accumulation and the tissue load of granulocytes and their histotoxic products in inflammatory processes. Neutrophil apoptosis may represent an important event in the control of intlamtnation. It has been assumed that granulocytes disintegrate to apoptotic bodies before their fragments are removed by local macrophages. Removal of neutrophils from the inflammatory site without release of granule contents is of paramount importance for cessation of inflammation. In conclusion, apoptotic cell death plays an important role in inflammatory processes and in the resolution of inflammatory reactions. The facts known at present should stimulate further research into the role of neutrophil, eosinophil and macrophage apoptosis in inflammatory diseases.


2018 ◽  
Vol 17 (4) ◽  
pp. 205-213
Author(s):  
Massimo Papi ◽  
Claudia Papi

In the last decades the possibility to diagnose a skin ulcer has greatly improved. We learnt that a consistent percentage of nonhealing ulcers may be caused by a microangiopathic disorder that has not been properly investigated and cured. Pathogenetically, we can distinguish 2 main groups: (1) ulcers due to inflammatory microangiopathy, mainly including cutaneous small and medium vessel vasculitis, pyoderma gangrenosum, and connective tissue diseases, and (2) ulcers due to occlusive microangiopathy. The group of microangiopathic occlusive ulcers is more heterogeneous and includes different disorders ranging from livedo vasculopathy to calciphylaxis, hydroxyurea-induced ulcers, antiphospholipid antibodies ulcers, and various other types. These conditions can induce thromboses or anatomo-functional occlusion of cutaneous microvessels. Despite different physiopathologic mechanisms, the ulcer resulting from a primitive microangiopathy may receive basic treatments that are in the complex similar to other pathogenetically different wounds, including MOIST-based local therapy and elastic compression when it is not contraindicated. Persistent inflammatory processes are increasingly demonstrated as responsible for the chronicity of many skin ulcers. New data concerning the biological phases of wound healing and the molecules that play crucial roles in this process suggested the use of new specific therapies. Some of them such as growth factors and platelet-rich plasma are prevalently used as topical biologic agents with variable benefits. In recent years, a new class of systemic anti-inflammatory molecules, better known as biologic drugs, have been introduced in the cure of chronic inflammatory diseases that can induce microangiopathic injuries and ulcerative complication. They enlarged the therapeutic options in case of nonresponder microangiopathic ulcers and could represent a future model of “pathogenetically based” therapy of skin ulcers.


2017 ◽  
Vol 23 (2) ◽  
Author(s):  
Natalya Drohomyretska

Hemomicrocirculatory system – is a complex structure that reacts in every pathological process even before the clinical period and takes the first blow. The study of microhemocirculation will provide an opportunity to solve the important for practical medicine questions of pathogenesis of many diseases, as for the prevention and treatment of regional disorders of blood circulation.The objective of the research is to study the state of the hemomicrocirculatory bed (HMCB) of adventitia of varicose veins of the small pelvis (VVSP) in women with chronic inflammatory processes of the organs of the small pelvis (CIPOSP).Materials and methods of research. To evaluate the restructuring of the HMCB of adventitia of VVSP, the operating material of 12 women of reproductive age was used. Mainly, there were pieces of the ovarian vein. The study of the HMCB in the vein wall was performed by the non-injecting method of silver impregnation according to V.V. Kupriyanov. To standardize the results, the condition of the HMCB of adventitia of the venous wall in norm was studied in 5 women of reproductive age, who died as a result of various traumas.Results of the research. After the performed studies, the structural-morphological changes of the HMCB of the adventitia of the small pelvis veins were revealed. The dilation of capillaries, postcapillaries, postcapillary venules was observed. The diameter of the vessels of the HMCB of the ovarian vein adventitia was: venule – 94.21 ± 1.38 μM in comparison with the norm – 48.78 ± 1.60 μM (p<0.001); post-capillary venules – 46.76 ± 1.04 μM in comparison with the norm – 28.29 ± 1.1.01 μM (p<0.001); the capillaries were 11.22 ± 0.14 μM in comparison with the norm – 8.24 ± 0.16 μM (p<0.05), arterioles – 29.02 ± 0.76 μM in comparison with the norm – 25.19 ± 1.15 μM (p<0.01). The architectonics of the arterioles is almost unchanged. Lumen of venules is filled with formed elements. The structure of capillaries is polymorphic. The capillary net was localized and concentrated or was formed as a thick planar net, the capillaries were expanded. There were arterio-venulous anastomoses. Endothelial nuclei are shortened. In some preparations, the diameter of the arterioles corresponded to the diameter of the collection venules.  Conclusions:1. The first discovered by us changes in HMCB of adventitia of varicose veins of the small pelvis in women with CIPOSP can be one of the pathogenetic links of the development and progression of the varicose vein itself, which in turn aggravates the course of chronic inflammation.      2. The timely appointment of drugs that improve microcirculation will enable to prevent the development of dystrophic changes in the vein wall, improve the course of chronic inflammatory processes and reduce or completely eliminate the syndrome of “chronic pelvic pain”.


Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1802
Author(s):  
Elena Munoz-Perez ◽  
Ainhoa Gonzalez-Pujana ◽  
Manoli Igartua ◽  
Edorta Santos-Vizcaino ◽  
Rosa Maria Hernandez

Considering the high prevalence and the complex pharmacological management of immune-mediated inflammatory diseases (IMIDs), the search for new therapeutic approaches for their treatment is vital. Although the immunomodulatory and anti-inflammatory effects of mesenchymal stromal cells (MSCs) have been extensively studied as a potential therapy in this field, direct MSC implantation presents some limitations that could slow down the clinical translation. Since the beneficial effects of MSCs have been mainly attributed to their ability to secrete a plethora of bioactive factors, their secretome has been proposed as a new and promising pathway for the treatment of IMIDs. Formed from soluble factors and extracellular vesicles (EVs), the MSC-derived secretome has been proven to elicit immunomodulatory effects that control the inflammatory processes that occur in IMIDs. This article aims to review the available knowledge on the MSC secretome, evaluating the advances in this field in terms of its composition, production and application, as well as analyzing the pending challenges in the field. Moreover, the latest research involving secretome administration in IMIDs is discussed to provide an updated state-of-the-art for this field. Finally, novel secretome delivery alternatives are reviewed, paying special attention to hydrogel encapsulation as one of the most convenient and promising strategies.


2021 ◽  
Vol 82 (1) ◽  
pp. 42-44
Author(s):  
V. F. Chikaev ◽  
N. A. Safina ◽  
O. D. Zinkevich ◽  
O. V. Gevorkyan

We have studied the level of antibacterial antibodies to E coli. Rg. mirabilis, Ps. aeruginosa, Bact. fragilis, St. aureus, as well as to the endotoxin of grammatical bacteria (glycolipid - HLP) by enzyme immunoassay in plasma in patients with varying degrees of prevalence of the pyoinflammatory process in the abdominal cavity.


2018 ◽  
Vol 19 (12) ◽  
pp. 3851 ◽  
Author(s):  
Drew Neavin ◽  
Duan Liu ◽  
Balmiki Ray ◽  
Richard Weinshilboum

The aryl hydrocarbon receptor (AHR) is a nuclear receptor that modulates the response to environmental stimuli. It was recognized historically for its role in toxicology but, in recent decades, it has been increasingly recognized as an important modulator of disease—especially for its role in modulating immune and inflammatory responses. AHR has been implicated in many diseases that are driven by immune/inflammatory processes, including major depressive disorder, multiple sclerosis, rheumatoid arthritis, asthma, and allergic responses, among others. The mechanisms by which AHR has been suggested to impact immune/inflammatory diseases include targeted gene expression and altered immune differentiation. It has been suggested that single nucleotide polymorphisms (SNPs) that are near AHR-regulated genes may contribute to AHR-dependent disease mechanisms/pathways. Further, we have found that SNPs that are outside of nuclear receptor binding sites (i.e., outside of AHR response elements (AHREs)) may contribute to AHR-dependent gene regulation in a SNP- and ligand-dependent manner. This review will discuss the evidence and mechanisms of AHR contributions to immune/inflammatory diseases and will consider the possibility that SNPs that are outside of AHR binding sites might contribute to AHR ligand-dependent inter-individual variation in disease pathophysiology and response to pharmacotherapeutics.


2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Samuel García ◽  
Carmen Conde

Poly(ADP-ribose) polymerase-1 (PARP-1) is a nuclear enzyme with a crucial role in the maintenance of genomic stability. In addition to the role of PARP-1 in DNA repair, multiple studies have also demonstrated its involvement in several inflammatory diseases, such as septic shock, asthma, atherosclerosis, and stroke, as well as in cancer. In these diseases, the pharmacological inhibition of PARP-1 has shown a beneficial effect, suggesting that PARP-1 regulates their inflammatory processes. In recent years, we have studied the role of PARP-1 in rheumatoid arthritis, as have other researchers, and the results have shown that PARP-1 has an important function in the development of this disease. This review summarizes current knowledge on the effects of PARP-1 in rheumatoid arthritis.


1962 ◽  
Vol 41 (2) ◽  
pp. 185-194 ◽  
Author(s):  
Bengt Skanse ◽  
Wilfried von Studnitz

ABSTRACT The metabolic effects of prolonged administration of thyrotrophic hormone were studied in 5 euthyroid subjects and in 1 patient who had been subjected to total thyroidectomy. Thyrotrophic hormone (TSH) had no effect in the thyroidectomized patient, thus showing that the metabolic effects were mediated by stimulation of the thyroid. In the euthyroid subjects the TSH caused an increase in thyroid activity as judged by the rise in basal metabolic rate (BMR) and serum protein-bound iodine (PBI) and the clinical symptoms. The administration of TSH resulted in: elevation of the erythrocyte sedimentation rate (ESR), and in an increase of the fibrinogen, haptoglobin, coeruloplasmin and total hexose content of the serum; an increase of α1-, α2-, and β2-globulins and smaller and less consistent changes in the albumin and β1- and γ-globulins, i. e. changes of the type seen in acute infections or acute inflammatory diseases; a fall in the total serum lipids, cholesterol and phospholipids, and less consistent changes in the α- and β-lipoproteins. During continued administration of TSH all the above mentioned metabolic effects tended to level off and/or disappear, probably owing to formation of antibodies. Withdrawal of TSH was followed by a rebound phenomenon, presumably because of diminished production of thyroid hormone. From the clinical point of view the possibility of increased thyroid function being a cause of elevated ESR and of the serum proteins changes resembling those seen in acute inflammatory processes should perhaps be considered.


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