Ultrasonic Inhaler for Antiseptic Treatment of Purulent Maxillofacial Wounds

Antibacterial activity of ultrasonic mist of the Anolit ANK was studied. The results of the study were used in local treatment of purulent wounds. A total of 41 patients with odontogenic facial phlegmon were tested in our clinic. Each patient was first treated surgically. Then antiinflammatory and antibacterial therapy was prescribed. During the postoperative period irrigation with Chlorhexidine solution 0.05% was used for local antiseptic treatment of 15 patients; 12 patients were treated with Anolit ANK solution, and 14 patients − with high frequency ultrasonic mist of Anolit ANK. The main clinical criteria were used to observe the dynamics of the inflammation process. The use of the ultrasonic mist of antiseptic Anolit ANK accelerates the healing of the wound. The quantity of expended local antiseptic is 10 times decreased. In spite of sophisticated anatomy of facial–neck wounds and due to minute size of mist particles, the antiseptic penetrates deep into the wound channel, thus producing higher therapeutic effect.     

Efficiency of Magnesium-Containing Preparation Polykatan in Therapy of Purulent Wounds

Local treatment with polykatan, a magnesium-containing drug based on bischofite mineral, promoted healing of infected skin wounds. Wound cleansing from bacteria was due to a direct antibacterial effect of the drug.     

Detection of Bacterial Pathogens in Purulent Clinical Specimens by Immunofluorescence Techniques

A technique is described which may be used to identify Haemophilus influenzae type b, Streptococcus pneumoniae, group A and B streptococci, and Staphylococcus aureus in smears of clinical specimens.     

PCTR1 Enhances Repair and Bacterial Clearance in Skin Wounds

Tissue injury elicits an inflammatory response that facilitates host defense. Resolution of inflammation promotes the transition to tissue repair and is governed, in part, by specialized pro-resolving mediators (SPM). The complete structures of a novel series of cysteinyl-SPM (cys-SPM) were recently elucidated, and proved to stimulate tissue regeneration in planaria and resolve acute inflammation in mice. Their functions in mammalian tissue repair are of interest. Here, nine structurally distinct cys-SPM were screened and PCTR1 uniquely enhanced human keratinocyte migration with efficacy similar to epidermal growth factor. In skin wounds of mice, PCTR1 accelerated closure. Wound infection increased PCTR1 that coincided with decreased bacterial burden. Addition of PCTR1 reduced wound bacteria levels and decreased inflammatory monocytes/macrophages, which was coupled with increased expression of genes involved in host defense and tissue repair. These results suggest that PCTR1 is a novel regulator of host defense and tissue repair, which could inform new approaches for therapeutic management of delayed tissue repair and infection.

Inflammation is a critical phase of the tissue repair program that aids in containment of pathogens and clearance of dead tissue and debris.^1,2 Neutrophils are among the first innate immune cells recruited to injured tissue, and they possess an armament of chemical mediators that facilitate pathogen eradication. Monocytes are subsequently recruited and differentiate into macrophages that assist in pathogen detection and killing, as well as efferocytosis (ie, clearance of apoptotic cells). Distinct monocyte/macrophage subsets are temporally reprogrammed to directly promote tissue matrix remodeling, vascularization, and re-establishment of protective epithelial barriers through the release of growth factors, cytokines, and lipid mediators.3, 4, 5 If the tightly coordinated temporal dynamics of inflammation and its subsequent resolution are altered, delayed tissue repair can manifest and lead to necrosis and susceptibility to ongoing infection with pathogenic microbes.^2,6 Indeed, altered tissue repair is associated with several chronic diseases and thus new approaches to stimulate tissue repair are urgently needed.6, 7, 8, 9Lipid mediators are enzymatically generated from polyunsaturated fatty acids in injured tissues and govern both the initial phases of inflammation (eg, leukocyte recruitment, activation), as well as the resolution phase.^10,11 A superfamily of structurally diverse specialized pro-resolving mediators (SPM), which include lipoxins, resolvins, protectins, and maresins, have emerged as key mediators of active resolution that engage immune cells via specific receptors to blunt excessive neutrophil recruitment and to expedite macrophage efferocytosis.¹¹ Several SPM, including lipoxins, E-series resolvins, and D-series resolvins, also actively participate in tissue repair and regeneration in distinct contexts, including the skin, intestine, skeletal muscle, eye, gut, and periodontium.12, 13, 14, 15, 16, 17 Importantly, SPM facilitate host defense by stimulating macrophages and neutrophils to phagocytose and kill bacterial pathogens.¹⁸A novel series of cysteinyl-SPM (cys-SPM) comprising peptide conjugates within the resolvin, protectin, and maresin families were discovered and were coined conjugates in tissue regeneration (CTRs) based on their roles in promoting tissue regeneration in planaria.18, 19, 20 The complete structures of these novel mediators were systematically elucidated, and stereochemical assignments were performed, which was facilitated by total organic synthesis.18, 19, 20 They are biosynthesized via conjugation of glutathione to epoxide intermediates involved in protectin (16S,17S-epoxy protectin), maresin (13S,14S-epoxy maresin), and resolvin (7S,8S-epoxy resolvin) biosynthesis, yielding protectin CTRs (PCTRs), maresin CTRs (MCTRs), and resolvin CTRs (RCTRs), respectively¹⁸ (Figure 1A). The glutathione-conjugated mediators are designated PCTR1, MCTR1, and RCTR1, whereas cleavage of the γ-glutamyl group yields PCTR2, MCTR2, and RCTR2. These products are subsequently converted to cysteine-containing PCTR3, MCTR3, and RCTR3. These cys-SPM have been identified in human and mouse tissues, including spleen, lymph nodes, and self-resolving inflammatory exudates, and actively promote resolution of acute inflammation in vivo.¹⁸ They have direct actions on human leukocytes and promote macrophage efferocytosis, as well as bacterial phagocytosis, to facilitate host defense.²⁰ These pro-resolving roles act in concert with their roles in promoting tissue regeneration.18, 19, 20 Recent studies confirm and extend the potent inflammation-resolving actions of cys-SPM in multiple injury contexts.21, 22, 23, 24, 25Open in a separate windowFigure 1Structure-activity analysis of cys-SPM in promoting human keratinocyte migration. A: Cys-SPM biosynthetic pathways and structures, depicting key epoxide intermediates involved in the biosynthesis of protectins (PD1 and PCTRs), D-series resolvins (RvD1, RvD2, and RCTRs), and maresins (MaR1, MaR2, and MCTRs). Right panel, assessment of closure in scratch-wounded monolayers of human primary keratinocytes stimulated with EGF (100 ng/mL) or structurally distinct synthetic cys-SPM (1 and 10 nmol/L; 24 hours). B: Representative images of control and PCTR1-treated keratinocytes at baseline and 24 hours after wounding, with the black dotted line indicating the cell border. C: Assessment of proliferation by 5-ethynyl-2′-deoxyuridine (EdU) incorporation in keratinocytes in the presence of full serum medium or indicated concentrations of PCTR1 for 24 hours. D: Measurement of cAMP accumulation in keratinocytes stimulated with PCTR1 (10 nmol/L). E: Assessment of closure in wounded keratinocytes stimulated with PCTR1 in the presence or absence of PKA inhibitor, H89 (5 μmol/L). Data are expressed as means ± SEM. n = 5 independent experiments (A); n = 10 to 13 replicates from 2 independent experiments (C); n = 4 replicates from 2 independent assays (D); n = 15 to 17 replicates from 3 independent experiments (E). ∗P < 0.05 by one-way analysis of variance followed by Dunnett''s post hoc tests (A, C, and E), or unpaired t-test (D).The actions of cys-SPM in mammalian tissue repair programs, including re-establishment of epithelial barriers, have yet to be addressed. Here, evidence is presented that PCTR1 directly stimulates migration of human keratinocytes in vitro which translates to accelerated closure of full-thickness skin wounds in vivo. Importantly, PCTR1 was produced in wounds infected with the common skin pathogen, Staphylococcus aureus, and PCTR1 accelerated bacterial clearance, suggesting novel roles of this SPM in both facilitating host defense, as well as engaging in tissue repair programs.     

Experimental Study of the Effects of Metal Nanoparticles on Tumor Growth and Bone Marrow Hemopoiesis

Metal (Zn, Cu, Fe) nanoparticles, particularly Zn, induce regression of transplanted sarcoma 37 and increase the percentage of dead and degenerated cells. Antitumor effect of metal nanoparticles was not associated with leukopenia or coarse bone marrow abnormalities, but differential leukocyte and bone marrow counts remained changed.     

Effect of a Composition Containing Chitosan Gel and a Bioregulator from Blood Serum on Healing of Purulent Wounds in Mice

We studied the effect of combined preparation on the basis of chitosan containing a bioregulator isolated from cattle serum in a concentration of 10^-10 mg/ml on healing of purulent wounds in mammals in vivo.     

Bacterial Contamination of Blood Products and the Value of Pre-Transfusion Testing

There has been a dramatic increase recently in the number of reports of septic episodes associated with both red cell and platelet concentrate transfusions. These reports suggest that transfusion-associated septic reactions may occur as often as 1 per 4000 platelet transfusions, however, the true incidence of the bacterial contamination of stored cellular blood components has not yet been established. Recently developed automated techniques for the detection of bacteria are much more rapid than direct plating techniques. Such rapid techniques can be used to monitor the sterility of cellular blood products with greater sensitivity than Gram staining; using a small aliquot of the blood product taken soon after collection. Using such equipment, the incidence of bacterial contamination of 15,838 random donor platelet concentrates collected over a six-month period was determined and evidence of bacterial contamination was found in 32. Seven were classified as confirmed, 10 as unconfirmed and 12 as non-confirmed positives. The confirmed positivity rate was thus 4.4 per 10,000. This rate represents the minimum incidence of bacterial contamination of platelet concentrates and the true rate is likely higher, as some of the unconfirmed positives are likely to have been found to be positives, had the original platelet concentrate been available for culture. The true positive rate is therefore estimated to be between 4.4 and 10.7 per 10,000. Given this rate of bacterial contamination, it is our contention that all platelet concentrate units be monitored for bacteriologic sterility prior to their issue. The cost of such screening would be of the same order of magnitude as that for each of the tests currently performed to screen donors for transfusion-transmitted diseases. The addition of a bacteriologic surveillance program could contribute significantly to a blood supply with reduced risk and would enable relevant scientific advances, such as the prolongation of the storage time to be fully implemented to optimize patient care as well as blood product utilization.     

Bacterial Contamination of Blood Products and the Value of Pre-Transfusion Testing

There has been a dramatic increase recently in the number of reports of septic episodes associated with both red cell and platelet concentrate transfusions. These reports suggest that transfusion-associated septic reactions may occur as often as 1 per 4000 platelet transfusions, however, the true incidence of the bacterial contamination of stored cellular blood components has not yet been established. Recently developed automated techniques for the detection of bacteria are much more rapid than direct plating techniques. Such rapid techniques can be used to monitor the sterility of cellular blood products with greater sensitivity than Gram staining; using a small aliquot of the blood product taken soon after collection. Using such equipment, the incidence of bacterial contamination of 15,838 random donor platelet concentrates collected over a six-month period was determined and evidence of bacterial contamination was found in 32. Seven were classified as confirmed, 10 as unconfirmed and 12 as non-confirmed positives. The confirmed positivity rate was thus 4.4 per 10,000. This rate represents the minimum incidence of bacterial contamination of platelet concentrates and the true rate is likely higher, as some of the unconfirmed positives are likely to have been found to be positives, had the original platelet concentrate been available for culture. The true positive rate is therefore estimated to be between 4.4 and 10.7 per 10,000. Given this rate of bacterial contamination, it is our contention that all platelet concentrate units be monitored for bacteriologic sterility prior to their issue. The cost of such screening would be of the same order of magnitude as that for each of the tests currently performed to screen donors for transfusion-transmitted diseases. The addition of a bacteriologic surveillance program could contribute significantly to a blood supply with reduced risk and would enable relevant scientific advances, such as the prolongation of the storage time to be fully implemented to optimize patient care as well as blood product utilization.     

Argocytes Containing Enzyme Nanoparticles Reduce Toxic Concentrations of Arginine in the Blood

A method for incorporation of arginase nanoparticles into mouse erythrocytes has been developed and the possibility of reducing blood arginine concentration in animals with experimental hyperargininemia with arginase-loaded erythrocytes (argocytes) has been studied. Argocyte infusion to animals with hyperargininemia led to a rapid decrease in blood arginine concentration within 1 h and this effect of argocytes persisted for at least 4 h. This was paralleled by an increase in plasma concentrations of urea and ornithine. Hence, plasma arginine is hydrolyzed by arginase incorporated into argocytes; argocytes are functionally active and can serve as a defense system in pathological hyperargininemia, while the method developed by us can be regarded as a new nanobiotechnology for medicine and veterinary.     

Novel Polymeric Nanoparticles Assembled by Metal Ion Addition

Potentially biodegradable graft polymer core‐shell nanoparticles assembling by addition of metal ions intended to be used for radionuclide and drug delivery purposes are described. With Cu²⁺ ions, the self‐assembly is slow (within minutes) with low efficiency. With Fe³⁺ ions the nanoparticles are formed immediately and are of convenient size for passive tumor accumulation by the enhanced permeation and retention effect. Full in vitro degradation of these particles is achieved with deferoxamine as a model of in vivo transchelation capacity.     

Discarding the Initial Aliquot of Blood Does Not Reduce Contamination Rates in Intravenous-Catheter-Drawn Blood Cultures

Although venipuncture is the preferred method for obtaining blood cultures, specimens often are obtained from intravenous catheters (IVC). For IVC-drawn blood cultures, some authorities recommend discarding the initial 5 to 10 ml of blood to reduce contamination and remove potential inhibitory substances. To determine whether this practice reduced contamination rates (CR), we assessed the results of IVC-drawn blood cultures for adults. Thirty milliliters of blood was obtained aseptically. The first 10 ml, rather than being discarded, was inoculated into an aerobic culture vial. Using a second sterile syringe, 20 ml of blood was obtained and inoculated in 10-ml aliquots to aerobic and anaerobic culture vials. Positive cultures were evaluated to assess clinical significance (true versus contaminant). Out of 653 IVC-drawn blood culture pairs, both vials were contaminated in 38 pairs (5.8%); only the “discard” vial was contaminated in 33 (5.1%); and only the “standard” vial was contaminated in 31 (4.7%). Overall CR were 10.9% for the discard vial versus 10.5% for the standard vial (P = 0.90). We conclude that discarding an initial aliquot of blood when obtaining blood cultures from IVCs does not reduce CR.The standard method for obtaining blood for culture is venipuncture using aseptic techniques. With greater utilization of intravenous access catheters (e.g., PICC, Hickman, etc.), blood cultures often are obtained from these devices, yet there is no standardized method for obtaining blood for culture by this technique. Several reports have demonstrated increased blood culture contamination rates (i.e., false-positive results) when blood cultures are obtained from catheters (4, 8, 10, 15), which, in turn, can lead to inappropriate antibiotic administration as well as additional unnecessary diagnostic testing. Some authorities recommend discarding the first 5 to 10 ml of blood when obtaining blood from intravenous catheters (IVCs) prior to inoculating the blood culture vials (17), whereas others do not (1, 9, 16). The purpose of discarding these aliquots of blood is to remove any substances that could potentially inhibit microbial growth (e.g., heparin) (6, 19) and to reduce blood culture contamination rates. However, there are few published systematic assessments of this issue, no consensus recommendations on how to draw blood cultures from an IVC, and no controlled comparative evaluations of different techniques to obtain blood culture samples from an IVC.It has been standard practice at our institution to discard the first 10 ml of blood prior to obtaining blood for culture from IVCs. If patients have repeated blood cultures, in which 10 ml of blood is discarded with each culture, nosocomial anemia may occur or worsen and result in added morbidity (1, 3, 11, 18, 21). To determine whether discarding the initial aliquot of blood from IVC-drawn blood cultures reduces contamination, we inoculated the initial 10-ml sample of blood that would have been discarded into an aerobic blood culture vial and compared contamination rates in these vials with contamination rates in the “standard” blood sample obtained for culture from the same patient.