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Background Clostridioides difficile infection (CDI) frequently complicates allogeneic hematopoietic stem cell (allo-HCT) and solid organ transplantation (SOT). Methods We retrospectively analyzed risk factors and outcomes of CDI occurring within 30 days of transplant. Results Between March 2010 and June 2015, 466 allo-HCT and 1454 SOT were performed. The CDI cumulative incidence (95% CI) was 10% (8-13) and 4% (3-5), following allo-HCT and SOT, respectively (p < .01), occurring at a median (range) 7.5 days (1-30) and 11 (1-30), respectively (p = .18). In multivariate analysis, fluoroquinolones use within 14 days pre-transplantation was a risk factor for CDI following allo-HCT (HR 4.06 [95% CI 1.31-12.63], p = .02), and thoracic organ(s) transplantation was a risk factor for CDI following SOT (HR 3.03 [95% CI 1.31-6.98]) for lung and 3.90 (1.58-9.63) for heart and heart/kidney transplant, p = .02. Compared with no-CDI patients, the length of stay (LOS) was prolonged in both allo-HCT (35 days [19-141] vs. 29 [13-164], p < .01) and SOT with CDI (16.5 [4-101] vs. 7 [0-159], p < .01), though not directly attributed to CDI. In allo-HCT, severe acute graft-versus-host disease (aGVHD) occurred more frequently in patients with CDI (33.3% vs. 15.8% without CDI, p = .01) and most aGVHD (87.5%) followed CDI. Non-relapse mortality or overall survival, not attributed to CDI, were also similar in both allo-HCT and SOT. Conclusions Early post-transplant CDI is frequent, associated with fluoroquinolones use in allo-HCT and the transplanted organ in SOT, and is associated with longer LOS in both the groups without difference in survival but with increased aGVHD in allo-HCT.

Mikhail Bulgakov is renowned for his challenge to the dry literary canons of the Soviet regime through his fantstical works of colorful content and unorthodox form, such as Sobach'e serd'tse (Heart of a Dog) and Master i Margarita. But Bulgakov is much mort than an exotic exception to Soviet puritanicalness. His works also include the highly practical and realistic, such as the tragic war-time works "Zapiski iungo vracha" (Notes of a Young Doctor) and Belaia gvardiia (The White Guad). Bulgakov's literary challenge to Soviet censorship also took direct forms. including two works that brazenly satire and examine the utterly taboo subjest of state censorship: the play, Bagrovyi ostrov (The Crimson Island) and Teaal'nyi roman (Theatrical Novel). Bulgakov's challenge to power also extendel to the epistolary, in the form of letters he sent to the Soviet government (and were read by Stalin) that contain attacks against the Soviet censorship bureau. In this real-life drama of Bulgakov versus Soviet censorship, we witness the icredible creativity and bravery of the artist, as well as discover his original and informative theory about how Soviet censorship operated. Let us begin our examina tion of this drama with the censorship bureau itself, how it first functioned and how it came to focus its sights on Bulgakov.

Quezado, Zenaide M. N., Charles Natanson, Waheedullah Karzai, Robert L. Danner, Cezar A. Koev, Yvonne Fitz, Donald P. Dolan, Steven Richmond, Steven M. Banks, Laura Wilson, and Peter Q. Eichacker.Cardiopulmonary effects of inhaled nitric oxide in normal dogs and during E. coli pneumonia and sepsis. J. Appl. Physiol. 84(1): 107–115, 1998.—We investigated the effect of inhaled nitric oxide (NO) at increasing fractional inspired O2concentrations ([Formula: see text]) on hemodynamic and pulmonary function during Escherichia coli pneumonia. Thirty-eight conscious, spontaneously breathing, tracheotomized 2-yr-old beagles had intrabronchial inoculation with either 0.75 or 1.5 × 1010 colony-forming units/kg of E. coli 0111:B4 (infected) or 0.9% saline (noninfected) in one or four pulmonary lobes. We found that neither the severity nor distribution (lobar vs. diffuse) of bacterial pneumonia altered the effects of NO. However, in infected animals, with increasing[Formula: see text] (0.08, 0.21, 0.50, and 0.85), NO (80 parts/million) progressively increased arterial[Formula: see text] [−0.3 ± 0.6, 3 ± 1, 13 ± 4, 10 ± 9 (mean ± SE) Torr, respectively] and decreased the mean arterial-alveolar O2 gradient (0.5 ± 0.3, 4 ± 2, −8 ± 7, −10 ± 9 Torr, respectively). In contrast, in noninfected animals, the effect of NO was significantly different and opposite; NO progressively decreased mean[Formula: see text] with increasing[Formula: see text] (2 ± 1, −5 ± 3, −2 ± 3, and −12 ± 5 Torr, respectively; P < 0.05 compared with infected animals) and increased mean arterial-alveolar O2 gradient (0.3 ± 0.04, 2 ± 2, 1 ± 3, 11 ± 5 Torr; P< 0.05 compared with infected animals). In normal and infected animals alike, only at [Formula: see text]≤0.21 did NO significantly lower mean pulmonary artery pressure, pulmonary artery occlusion pressure, and pulmonary vascular resistance index (all P < 0.01). However, inhaled NO had no significant effect on increases in mean pulmonay artery pressure associated with bacterial pneumonia. Thus, during bacterial pneumonia, inhaled NO had only modest effects on oxygenation dependent on high[Formula: see text] and did not affect sepsis-induced pulmonary hypertension. These data do not support a role for inhaled NO in bacterial pneumonia. Further studies are necessary to determine whether, in combination with ventilatory support, NO may have more pronounced effects.

We examined serial changes in total body oxygen consumption (Vo2) in a permanently tracheotomized canine sepsis model. On Day 0, beagles had an Escherichia coli-infected (septic) or sterile (control) clot surgically placed in the peritoneum. During the 21-d study, 10 of the 16 septic animals and none of the six control animals died (p = 0.02). After clot placement septic versus control animals had decreased mean arterial blood pressure (mm Hg; Day 1: 106 versus 128, p = 0.055; Day 2: 95 versus 125, p = 0.004, respectively) and left ventricular ejection fraction (Day 1: 0.44 versus 0.69, p = 0.0006; Day 2: 0.33 versus 0.57, p = 0.0001, respectively). Despite significant lethality and cardiovascular dysfunction, in the septic group on Days 1 and 2, septic versus control animals had no significant differences in mean metabolic cart measured (Vo2DIR, ml/kg/min; Day 1: 11.9 versus 12.4, p = 0.81; Day 2: 14.2 versus 13.5, p = 0.72, respectively) and intravascular catheter calculated (Vo2INDIR, ml/kg/min; Day 1: 11.2 versus 11.2, p = 0.99; Day 2: 12.8 versus 15.4, p = 0.49, respectively). On Day 1 in septic and control animals, volume infusion produced increases (p < 0.001) in oxygen delivery (Do2). In septic and control animals these changes in Do2 were similar and were associated with similar increases in Vo2DIR (p = 0.001), and Vo2INDIR (p = 0.001). In fact, at all time points studied (baseline, Day 1, 2, and 21), both before and after volume infusion, levels of Do2, Vo2DIR, and Vo2INDIR did not differ between septic and control animals, nor did they differ between septic survivors and nonsurvivors. Because levels of Vo2DIR and Vo2INDIR were similar in both groups, we pooled data from septic and control animals. Throughout the study, Vo2 showed a moderate association with Vo2INDIR (r = 0.55, p = 0.003), but mean Vo2DIR was lower at baseline (p = 0.001) and on Day 21 (p = 0.07) and greater on Day 2 (p < 0.01). In summary, our techniques, which detected small changes in both Vo2DIR and Vo2INDIR occurring with volume infusion, did not demonstrate differences in these parameters comparing control and septic animals. These results in euvolemic septic animals suggest that total body Vo2 may not reflect pathogenetic mechanisms during sepsis and septic shock. Furthermore, these results suggest that although the level of total body Vo2 may reflect the effects of therapeutic interventions such as volume loading, it should not itself serve as a therapeutic target.

This study examined the effect of monoclonal antibody (MAb) directed against leukocyte CD11b/18 glycoprotein complex (904MAb) on cardiopulmonary injury induced by tumor necrosis factor (TNF), and death. Eighteen 2-yr-old, purpose-bred beagles with chronic tracheostomies were challenged with TNF (60 micrograms/kg of body weight) intravenously. Nine of 18 animals were treated with 0.5 to 1.0 mg/kg of body weight 904MAb intravenously 45 min before and 12, 36, and 48 h after TNF infusion. Serial femoral and pulmonary arterial catheter hemodynamics, blood gas analysis, and radionuclide cineangiographic left ventricular ejection fractions (EF) were done before and after a fluid challenge. Serial bronchoalveolar lavages (BAL) with cell and protein analysis also were performed using the chronic tracheostomies. Compared with animals given TNF alone, animals treated with 904MAb did not differ in overall survival (TNF alone, 2/9; 904MAb, 3/9); however, the group of animals treated with 904MAb had significantly (p less than 0.01) fewer deaths within the first 30 h of TNF challenge. At 4 h after TNF challenge, all animals had significantly (p less than 0.05) reduced PaO2 after fluid challenge; however, animals given 904MAb (compared with animals given TNF alone) had significantly (p less than 0.05) smaller reductions in PaO2. Throughout the study, animals given 904MAb before TNF or TNF alone had similar changes in cardiac index, mean arterial pressure, EF, and BAL protein and neutrophil concentration. Thus, MAb directed against the leukocyte CD11b/18 glycoprotein complex prolonged survival and reduced the hypoxemia occurring after TNF challenge, but this antibody did not improve overall survival or cardiopulmonary function.(ABSTRACT TRUNCATED AT 250 WORDS)

The future looked bright for the thirty-year-old graduate student as he considered which path to take. He had won medals at school, taken a degree from the prestigious Institute of Foreign Trade, studied for a year in Beijing, and worked for three years at the Ministry of Foreign Trade. Now he had successfully defended a dissertation on the finances of the People's Republic of China. He was married, a new father, and on the fast track for a successful career in the diplomatic corps or another elite profession. "But this was 1961, and there then occurred the break between the Soviet Union and China. The Higher Attestation Committee did not confirm my dissertation. All institutions that worked with China were liquidated and I was forced to look for a job. That's how I came to Glavlit." So began, "to a certain degree by chance," the censorship career of Vladimir Solodin. Within ten years Solodin would rise from a trainee-censor in international relations to a member of the ruling council of the Soviet literary censorship, Glavlit. From 1971 until 1991, Solodin directed Glavlit's Fourth Department of "artistic and political literature," making him responsible for the daily operations of Soviet censorship and the training of new censors. The senior censorship official after two or three Kremlin appointees, Solodin was "the highest professional," as he put it, and unofficially but widely known as the "Chief Censor." After the fall of the Soviet Union in 1991, Solodin became chief of the prosecutor's office of the Ministry of Print and Information. No longer could he summon editors and writers to his office for "consultations." In the new Russia, Solodin petitioned Russian courts to move against violators of new Russian laws that prohibited publication of "indecent" and "prejudicial" materials. But as Russia soon began to stumble on the path of democracy, it would once again call upon Solodin to serve, for just a few more hours, as Chief Censor. By late September 1993 the executive and legislative branches of the new Russian Federation had worked themselves to the brink of civil war. For two weeks troops loyal to President Yeltsin laid siege to a parliament building occupied by heavily armed legislators and their supporters. "I was on the side of President Yeltsin because at that time that was the only grouping in the country that stood for some sort of order," recalled Solodin. On the afternoon of 3 October the warring began. What sparked the actual fighting is the source of controversy. The answers may never be known since an official investigation was never undertaken-a little-known part of the deal that produced the general amnesty of political prisoners of 23 February 1994. On Saturday, 2 October, the day before the fighting began at the parliament, the