A new aspect of in vitro antimicrobial leukocyte- and platelet-rich plasma activity based on flow cytometry assessment

The current literature suggests that the antibacterial effect of leukocyte- and platelet-rich plasma (L-PRP) is directly related to platelet and leukocyte concentrations. The aim of this study was twofold: first, to evaluate the antimicrobial effect of L-PRP against selected bacterial strains in vitro, and second, to correlate this effect with leukocyte and platelet content in the final concentration. Blood was collected from 20 healthy males, and L-PRP, acellular plasma (AP), and autologous thrombin were consecutively prepared. Flow cytometry analysis of the blood, L-PRP, and AP was performed. The L-PRP gel, liquid L-PRP, and thrombin samples were tested in vitro for their antibacterial properties against seven selected bacterial strains using the Kirby–Bauer disk-diffusion method. There was notable antimicrobial activity against selected bacterial strains. No statistically significant correlations between antimicrobial activities and the platelet concentration in L-PRP were observed. Statistically significant positive correlations between selected leukocyte subtypes and antimicrobial activity were noted. A negative correlation was found between elevated monocyte count and antimicrobial activity of L-PRP against one bacterial strain studied. L-PRP possesses antimicrobial activity and can be potentially useful in the fight against certain postoperative infections. The bactericidal effect of L-PRP is caused by leukocytes, and there exists a relationship among selected leukocyte subtypes and L-PRP antimicrobial activity.     

Olmesartan is an angiotensin II receptor blocker with an inhibitory effect on angiotensin-converting enzyme.

Angiotensin II receptor blockers (ARBs) are widely used for the treatment of hypertension. It is believed that treatment with an ARB increases the level of plasma angiotensin II (Ang II) because of a lack of negative feedback on renin activity. However, Ichikawa (Hypertens Res 2001; 24: 641-646) reported that long-term treatment of hypertensive patients with olmesartan resulted in a reduction in plasma Ang II level, though the mechanism was not determined. It has been reported that angiotensin 1-7 (Ang-(1-7)) potentiates the effect of bradykinin and acts as an angiotensin-converting enzyme (ACE) inhibitor. It is known that ACE2, which was discovered as a novel ACE-related carboxypeptidase in 2000, hydrolyzes Ang I to Ang-(1-9) and also Ang II to Ang-(1-7). It has recently been reported that olmesartan increases plasma Ang-(1-7) through an increase in ACE2 expression in rats with myocardial infarction. We hypothesized that over-expression of ACE2 may be related to a reduction in Ang II level and the cardioprotective effect of olmesartan. Administration of 0.5 mg/kg/day of olmesartan for 4 weeks to 12-week-old stroke-prone spontaneously hypertensive rats (SHRSP) significantly reduced blood pressure and left ventricular weight compared to those in SHRSP given a vehicle. Co-administration of olmesartan and (D-Ala7)-Ang-(1-7), a selective Ang-(1-7) antagonist, partially inhibited the effect of olmesartan on blood pressure and left ventricular weight. Interestingly, co-administration of (D-Ala7)-Ang-(1-7) with olmesartan significantly increased the plasma Ang II level (453.2+/-113.8 pg/ml) compared to olmesartan alone (144.9+/-27.0 pg/ml, p<0.05). Moreover, olmesartan significantly increased the cardiac ACE2 expression level compared to that in Wistar Kyoto rats and SHRSP treated with a vehicle. Olmesartan significantly improved cardiovascular remodeling and cardiac nitrite/ nitrate content, but co-administration of olmesartan and (D-Ala7)-Ang-(1-7) partially reversed this anti-remodeling effect and the increase in nitrite/nitrate. These findings suggest that olmesartan may exhibit an ACE inhibitory action in addition to an Ang II receptor blocking action, prevent an increase in Ang II level, and protect cardiovascular remodeling through an increase in cardiac nitric oxide production and endogenous Ang-(1-7) via over-expression of ACE2.     

Chromogalactography preceding ductal-lobular unit excision for nipple discharge--with special reference to diagnostic galactography and histology

Between 1981-88, 223 surgical interventions were performed in cases of pathologic breast secretion after exclusion of extra-mammary aetiology. The milk duct was identified by pre-operative chromogalactography, followed by a selective excision of the ductal-lobular unit. In 36 cases (16.1%), however, neither spontaneous nor provocable secretion remained after diagnostic galactography, so that a segment resection was required. In all tissue specimens, the cause of the pathologic secretion was found histologically; most often, it was fibrocystic disease or solitary intraductal papilloma (21.5% each). In 32.3% of the specimens, findings with a prospective significance (papillomatosis, carcinoma in situ or invasive carcinoma) were discovered and further operative treatment was initiated. The colour of the discharge allowed no prediction of the histological findings. In 28.6% (8/28) of the carcinomas, secretion was bilateral. In 46.4% of the specimens containing carcinoma, papillomatosis was also detected; vice versa, papillomatosis was associated with carcinoma in 22.8%. The recurrence rate of 1.6% indicates the efficiency of this method in removing the pathology. The diagnostic value of galactography for the prediction of findings with a prospective significance was considerably reduced by a rate of 37.5% false-negatives; therefore, we have decided to omit diagnostic galactography in our patients. Now, provided extra-mammary causes of the nipple discharge have been excluded and mammography has been inconspicuous, a selective excision of the ductal-lobular unit is performed after preoperative chromogalactography.     

Laryngotracheal resection and reconstruction for subglottic stenosis.

Eighty patients with inflammatory stenoses of the subglottic larynx and upper trachea were treated by single-stage laryngotracheal resection and reconstruction. Fifty stenoses originated from postintubation lesions (endotracheal tubes, tracheostomy, cricothyroidostomy), 7 originated from trauma, 19 were idiopathic, and 4 were miscellaneous. Repair consisted of resection of the anterolateral cricoid arch in all patients, plus resection of posterior laryngeal stenosis where present, with salvage of the posterior cricoid plate, appropriate resection and tailoring of the trachea, and primary anastomosis using a posterior membranous tracheal wall flap to resurface the bared cricoid cartilage in 31 patients. One postoperative death resulted from acute myocardial infarction. Long-term results were excellent in 18 patients, good in 48, satisfactory in 8, and failure in 2. Three additional patients had good results at discharge but were followed up for less than 6 months.     

Therapy of primary fallopian tube cancer--a retrospective study of 30 cases]

Between the years 1968-1988 30 patients with primary carcinoma of the fallopian tube were treated in the Department of Obstetrics and Gynecology of the University of Kiel. In 27 cases the initial treatment consisted of total abdominal hysterectomy and bilateral salpingo-oophorectomy. In 3 cases where the patients had undergone surgical treatment in another hospital a second operation for completion was performed. 2 patients received no further treatment after surgery. Postoperative radiotherapy was given to 20 patients and a combined treatment with radiation and polychemotherapy was implemented in 5 cases. Postoperative treatment in 3 patients was poly-chemotherapy alone. The 5-year-survival rate taking all tumor stages and modes of therapy employed into consideration was 36.7%. In analysing the survival rate for small numbers as directly related to postoperative treatment a 5-year-survival rate for radiotherapy of 35% (7/20) and for radiation therapy plus poly-chemotherapy of 40% (2/5) was found. After operative treatment followed by poly-chemotherapy alone one of three patients survived after 5 years.     

Molecular cloning and sequencing of a cDNA for olfactory marker protein.

cDNA clones corresponding to mRNA for rat olfactory marker protein (OMP) were isolated from a cDNA library. The library was constructed from olfactory mucosa poly(A)+ RNA enriched for OMP mRNA and cloned into a pBR322-derived plasmid, pMG5. OMP cDNA clones were detected by using a 17-base oligonucleotide probe that contained all 16 possible sequences coding for a known partial amino acid sequence of rat OMP. The identity of these clones was confirmed by hybrid-selected translation and nucleotide sequencing. The sequence of one clone was determined and contained the complete OMP coding region of 486 nucleotides followed by 1630 nucleotides of the 3' untranslated region. The 3' untranslated region included the polyadenylylation signal 16 nucleotides upstream of the poly(A) tail. No other ATG-initiated open reading frame larger than 20 codons was present in register. RNA blot analysis of olfactory mucosa poly(A)+ RNA using this clone as a probe indicated that the level of OMP mRNA, but not its size, declined significantly within a few days following olfactory bulbectomy. OMP mRNA was not detected in 14 nonolfactory rat tissues. Surprisingly, a small amount of OMP mRNA was observed in olfactory bulb. The presence of OMP mRNA in olfactory bulb was confirmed by in vitro translation and immunoprecipitation. These results suggest either that a previously undescribed population of neurons in the olfactory bulb synthesize OMP or that OMP mRNA is transported to the bulb by axonal transport.     

Spontaneous coronary artery dissection mimicking aortic dissection

A 51-year-old woman suffered rapidly irreversible cardiogenic shock with left hemiparesis. Transesophageal echocardiography, which represents an essential imaging tool in the emergency room, ruled out aortic dissection involving branch vessels but did not allow an in vivo diagnosis of spontaneous coronary dissection. The in vivo diagnosis of spontaneous coronary dissection is rather difficult because of the dramatic clinical presentation and selective coronary angiography requirement.     

Esophagopleural Fistula: A Complication of Chest Intubation for Empyema

This report documents the first recorded patient in the recent literature with an esophageal perforation and an esophagopleural fistula following chest intubation for empyema. It was treated successfully by conservative method with feeding gastrostomy. It is important to realize that tube thoracostomy drainage is not an innocuous procedure and to be alert to this complication, especially in the presence of empyema.