A typical inverted U-shaped relationship exists between the cell survival and freezing rates [25]. Therefore, an optimum freezing rate should be slow enough to prevent intracellular ice formation and fast enough to minimize the osmotic shock [26]. In general, it is expected that slow freezing rates result

in the dehydration of cells to compensate for the greater extracellular salt concentration due to ice formation at sub-zero temperatures. Consequently, the intracellular salt concentration increases lead to osmotic shock (solution effect). However, rapid freezing rates would result in cells that do not have sufficient time to dehydrate, leading to intracellular ice formation Epacadostat concentration upon freezing [4]. Straws volume may also affect the semen quality, once the surface-to-volume ratio influences the velocity of latent heat dissipation, affecting the sperm thawing procedure [33]. For swine, the domestic animal closely related to the peccaries [9], the type of package used to freeze–thaw semen usually affects sperm motility and viability [6]; but, by now, only 0.25 mL straws were used for freezing the semen of collared peccaries [7], [8] and [34]. VX-765 manufacturer The objective of this study was to verify the effect of different freezing curves, straw sizes, and thawing rates in order to improve the protocol for collared

peccary semen cryopreservation. The ethics committee of the UFERSA has approved the experimental protocols as well as the animal care procedures adopted (Process no. 23091.0253/114). The reagents used in the present study were obtained from Sigma–Aldrich (St. Louis, MO, United States). A total of eight sexually mature male collared peccaries, aged 40.7 ± 1.6 months with a weight of 22.5 ± 2.8 kg were included in the study. The animals belonged to the Centre of Multiplication of Wild Animals from UFERSA, located in northeast Brazil (Mossoró, RN, Brazil; 5° 100′ S, 37° 100′ W). The region is subject

to a typical semi-arid climate with an average annual temperature of 27 °C. The animals were isolated Sitaxentan from the females for a period of six months prior to the commencement of the study and were kept under a 12 h natural photoperiod. Subsequently, they were divided into groups of four and five animals and maintained outdoors in paddocks (20 × 3 m) with a covered area measuring 3 × 3 m. The animals were fed on a diet of sow food and fruits, and water was provided ad libitum. The animals were kept in fasting condition for 12 h prior to the start of the experiments. They were then physically restrained using a hand net and anesthetized using intravenous administration of propofol (Propovan®, Cristalia, Fortaleza, Brazil), given as a bolus (5 mg/kg) [36]. When the animal showed signs of awakening, additional propofol (approximately 1.25 mg/kg) was given to prolong the anesthesia.

9 vs 6.1 months; hazard ratio [HR]: 0.67, p = .012) and in patients selleck screening library of Asian origin (median survival, 9.5 vs 5.5 months; HR: 0.66, p = .01). A later exploratory biomarker analysis found a numeric (but not statistically significant) RR benefit with gefitinib in patients with EGFR protein-expressing tumors as well as those with high EGFR copy numbers. Patients whose tumors expressed EGFR protein also had a numerically greater survival benefit (HR: 0.77; p = .126) compared

with those whose tumors did not express EGFR (HR: 1.57; p = 0.14). The presence of somatic mutations in EGFR Exons 19 and 21 also appeared to predict response (RR, 37.5% vs 2.6%; p-value not reported) [34]. Another phase 3 trial evaluating gefitinib in lung cancer called INTEREST (Iressa Non-small-cell lung cancer Trial Evaluating REsponse and Survival against Taxotere), conducted in 1466 patients with NSCLC who had received 1 or 2 prior chemotherapy

regimens, found gefitinib to be non inferior for survival (median OS of 7.6 months; 1-year survival of 32%) compared with docetaxel, and offered improved tolerability and patient quality of life. Preplanned subgroup analyses found one significant difference between the treatment groups: patients who had received 2 prior chemotherapy regimens had better survival with docetaxel than with gefitinib (p = .031). Overall, among patients taking gefitinib, 2.2% had grade 3/4 hematologic Pirfenidone nmr AEs, whereas docetaxel-treated patients had a 58.2% incidence of grade 3/4 neutropenia and a 42.3% incidence of grade 3/4 leukopenia [35]. Erlotinib has shown a significant improvement in median survival, quality of life, and related symptoms in an unselected population of advanced and metastatic NSCLC patients in the second or third-line setting and most recently in maintenance therapy. National Cancer Institute of Canada Clinical Trials Group conducted a phase III randomized trial, named BR.21,

in which erlotinib was compared with placebo in stage III/IV NSCLC patients who had failed first- or second-line chemotherapy. A total of 731 patients Thiamet G were randomized in a 2:1 ratio to receive either erlotinib at 150 mg/day or placebo. Those patients had metastatic NSCLC that had previously been treated with one standard chemotherapy regimen (50% of patients) or with two chemotherapy regimens (50% of patients). Almost all patients received platinum-based chemotherapy. The OR rate was 8.9% in the erlotinib arm and 1% in the placebo group. The median durations of response were 7.9 months and 3.7 months, respectively. The median over-all survival time was 6.7 months for those in the erlotinib regimen compared with 4.7 months for those in the placebo arm. ORs were more frequent in women (14% vs 6%), in patients with adenocarcinoma, as compared with other histotypes (14% vs 4.1%), and in patients without a smoking history (25% vs 4%) [36].

, 2003, Xu et al., 2003 and Shu et al.,

2012). This macrophage proliferation, coupled with increased TLR4 and other pattern recognition receptors on adipocytes, leads to an increase in the pro-inflammatory cytokine profile (Hotamisligil et al., 1993, Hotamisligil et al., 1995, Uysal et Daporinad al., 1997 and Shu et al., 2012). Increased pro-inflammatory cytokines, adipokines, and fatty acids then have downstream effects on liver and muscle, which contribute to systemic insulin resistance (Shu et al., 2012). Pro-inflammatory cytokines, such as tumor necrosis factor (TNF)α activate serine kinases that directly and indirectly phosphorylate insulin receptor substrate (IRS) 1 and 2, resulting in a reduced ability of insulin to stimulate phosphatidylinositol-3 kinase (PI-3K)-dependent pathways that normally result in glucose uptake and metabolism (Hirabara et al., 2012). Feeding-related pathways in the hypothalamus are also disrupted by inflammation, with insulin and leptin less able to suppress hunger and feeding, further contributing to the maintenance of a high fat diet and thus obesity Trametinib (Thaler and Schwartz, 2010). Obesity- and high fat diet-associated systemic inflammation was identified some time ago, with early reports suggesting obese humans and high fat diet-fed rodents

have elevated circulating pro-inflammatory cytokines compared with controls, and macrophage infiltration into the WAT (Pickup and Crook, 1998, Weisberg et al., 2003 and Wellen and Hotamisligil, 2003). The suggestion that obesity can also result in central inflammation, however, Anacetrapib is a relatively recent one. In 2005, de Souza and colleagues showed high fat diet elevates the expression of pro-inflammatory cytokines and activation of the pro-inflammatory

transcription factor nuclear factor κB (NFκB) in the hypothalamus (De Souza et al., 2005). Several other investigations followed, suggesting high fat diet can cause hypothalamic inflammation and that this inflammation can interrupt normal feeding- and metabolism- related signaling. Thus, high fat feeding leads to infiltration and activation of microglia (the brain’s resident macrophages) in the hypothalamus, activation of inflammatory signaling, and increases in local inflammatory mediators such as cytokines (Fig. 1) (De Souza et al., 2005, Zhang et al., 2008, Milanski et al., 2009, Posey et al., 2009 and Thaler et al., 2012). Importantly, this central inflammation can actually contribute to leptin and insulin resistance, favoring weight gain and maintaining an elevated body weight (De Souza et al., 2005 and Posey et al., 2009). As with systemic increases in pro-inflammatory cytokines, increases in TNFα, IL-6 etc.

It has been suggested that the osteocyte processes might be attached directly to the canalicular wall by β3 integrins at the apex of infrequent, previously

unrecognized canalicular projections [43]. A theoretical model was developed that predicts that the tensile forces acting on these integrins can be as large as 15 pN, buy Alisertib and thus provide stable attachment in the range of physiological loading [20]. The model also predicts that axial strains caused by the sliding of actin microfilaments relative to the fixed attachments are two orders of magnitude greater than whole-tissue strains thereby producing local membrane strains in the cell process that can exceed 5%. In vitro experiments indicated that membrane strains of this order are large enough to open stretch-activated cation channels [74]. It is likely that stretch-activated ion channels play a role in the transduction of mechanical stimuli into a chemical response in osteocytes. A well known early response to mechanical stimulation of osteocytes and other mechanosensitive bone cells in vitro is an increase in intracellular calcium concentration [75], which could well be caused by opening of stretch-activated ion channels. Although no direct evidence exists that transient receptor potential (TRP) channels are stretch-activated ion channels, it is an idea that has often been

put forward. In MLO-Y4 osteocytes the Venetoclax nmr calcium response to mechanical stimulation can be partially blocked by Gd3 + [76], suggesting that some kind of TRP channel is involved in this response. Little is known about TRP channel expression in osteocytes, only TRPV6 is known to be expressed at low levels in murine osteocytes [77]. So far the involvement of specific ion channels in the mechanoresponse of osteocytes has not been elucidated. As described

above, actin microfilaments in the osteocyte cell extensions may slide relative to the fixed attachments. As a result, stretch-activated ion channels may be pulled open, since such channels are connected to the cytoskeleton. On the outside of the osteocyte Methisazone process any stretch-activated ion channels may also be connected to the extracellular matrix via tethers, further enabling the opening of ion channels. Such tethering filaments appear to be absent in the pericellular space surrounding the cell body, likely due to the wide pericellular space (~ 1 μm) between the cell membrane and the wall of the lacuna. In contrast, the pericellular space surrounding the cell process on average is 80 nm [32]. You et al. [78] were the first to propose that there were regularly spaced tethering filaments that attached the cell processes to the canalicular wall. They postulated that the flow through the pericellular matrix, which was supported by these tethers, would put them in tension creating a hoop strain on the cell process membrane.

, 2013a, Eickhoff et al., 2008, Palomero-Gallagher BMS-354825 ic50 et al., 2009, Zilles et al., 2002a and Zilles et al., 2004). Autoradiographic labeling of the sections with tritium [3H]-labeled ligands was performed according to standardized protocols (Zilles, Schleicher, et al., 2002; Supplementary Table 1). The experimental procedure included three successional steps:

1) Pre-incubation to rehydrate the tissue and remove endogenous ligands and other substances which potentially bind to the receptors. 2) Main incubation to label the receptors with only the respective tritiated ligands in nM, or with the tritiated ligands in presence of the respective non-labeled competitors in μM. By comparing these two experimental conditions, the specific binding could be calculated: The incubation with only the tritiated ligand denoted the total binding, whereas the incubation with the additional non-labeled competitor showed the non-specific binding. The specific binding was calculated as the difference between total binding and non-specific binding. It was less than 5% in all cases. MLN0128 supplier 3) Final rinsing to stop binding and remove superfluous radioactive ligands. Radioactively labeled

sections were co-exposed with [3H]-plastic scales of known radioactivity against [3H]-sensitive films for 4–18 weeks. The developed films were digitized using a CCD-camera. Gray values of the digitized images were transformed into radioactivity concentrations by a non-linear transformation computed from the gray values of the co-exposed plastic standards of known radioactivity concentrations. These linearized autoradiographs 4��8C were contrast enhanced, and color coded in a spectral color sequence for a better visualization of regional differences. Regions of interest were selected and defined using cyto- and receptor architectonical as well as landmark-based identification as described in the literature (Amunts et al., 2010, Amunts et al., 1999, Brodmann, 1909, Caspers et al., 2013a, Caspers

et al., 2013c, Eickhoff et al., 2007, Friederici et al., 2009, Geyer et al., 1997, Makuuchi et al., 2009, Morosan et al., 2005, Palomero-Gallagher et al., 2009, Scheperjans et al., 2005 and Zilles and Amunts, 2010). Receptor densities were extracted from the regions of interest based on a previously described densitometric analysis (Zilles, Schleicher, et al., 2002). For each of the examined receptor types, profiles oriented vertically to the cortical surface and covering the full cortical width were extracted from the linearized autoradiographs (Zilles, Schleicher, et al., 2002). The area below the profile quantifies the mean areal density in fmol/mg protein. Densities were averaged over three sections and four hemispheres, and provided the mean value for each receptor in each area. These values were registered for each area separately in a polar plot.

U chorych bez poprawy po odstawieniu antybiotyku wyzwalającego biegunkę lekiem z wyboru jest metronidazol (30 mg/kg masy ciała/dobę

w czterech dawkach, stosowany co najmniej przez 10 dni doustnie lub wyjątkowo dożylnie – gdy niemożliwa jest droga doustna). W ciężkich postaciach zapalenia jelit, przy obecności błon rzekomych w badaniu endoskopowym, braku poprawy po leczeniu metronidazolem stosuje się wankomycynę (40 mg/kg masy ciała/dobę w czterech dawkach doustnie lub we wlewie doodbytniczym). Podobną skuteczność wankomycyny podawanej doustnie po wcześniejszej nieskutecznej this website terapii metronidazolem wykazano u opisanych przez nas pacjentów III i IV. W najcięższych postaciach biegunki Clostridium difficile należy stosować metronidazol dożylnie wraz z wankomycyną doustnie lub we wlewie doodbytniczym. U około 20% chorych z rzekomobłoniastym zapaleniem jelita grubego dochodzi do nawrotu choroby, zazwyczaj po 3–21 dni od zakończenia leczenia. U połowy chorych nawrót powodowany jest przez ten sam szczep bakterii [10]. Tłumaczy się to słabą odpowiedzią układu odpornościowego pacjenta i zbyt małym poziomem przeciwciał wytworzonych a pełniących funkcję antytoksyn. Ryzyko nawrotu wzrasta wraz z kolejnym nawrotem

choroby. Zaleca się stosowanie tego samego leku, za pomocą którego wyleczono pierwszy epizod selleck inhibitor choroby, za wyjątkiem, gdy jest to przebieg cięższy, wtedy wskazane jest stosowanie wankomycyny [10]. W leczeniu nawrotów wankomycynę można stosować w SPTBN5 wysokich dawkach, tj. 2 g/dobę przez 10 dni i następnie dawki 125–500 mg podawane co 3. dzień przez 4 tygodnie. U opisanego przez nas pacjenta I także po 10 dniach wystąpił nawrót dolegliwości, zastosowano ponownie antybiotyk, którego użyto przy pierwszym rzucie choroby z poprawą kliniczną. W przypadku nawrotu choroby istnieją doniesienia o innych możliwościach terapeutycznych z zastosowaniem rifaxyminy, fidaxomicyny, teikoplaniny oraz wlewek doodbytniczych z zastosowaniem stolca osób zdrowych [15], [16], [17] and [18]. Niewątpliwie metody te wymagają dalszych

badań celem oceny skuteczności tego postępowania. Rzekomobłoniaste zapalenie jelita grubego może prowadzić do toksycznego rozdęcia okrężnicy (megacolon toxicum) lub perforacji jelit, które wymagają leczenia chirurgicznego. Ze względu na możliwość wystąpienia biegunki w wyniku antybiotykoterapii przy prowadzeniu racjonalnej antybiotykoterapii u dzieci nieocenioną rolę ochronną spełniają probiotyki. Znane od początku XX wieku probiotyki jako żywe, wyselekcjonowane szczepy mikroorganizmów, stosowane w odpowiednich ilościach wywierają ochronny efekt na organizm. W Polsce Grupa Ekspertów na podstawie metaanaliz, badań z randomizacją prowadzonych na całym świecie, ustaliła stanowisko dotyczące zaleceń stosowania poszczególnych szczepów probiotycznych w profilaktyce biegunki związanej z antybiotykoterapią u dzieci [1].

As a consequence of this, DSBs are generated in the vicinity of collapsed replication forks and this activates a DDR and forces cells to undergo senescence [48 and 49]. OIS not only functions as a tumour suppressing mechanism in animal model systems [50], but also cells with features Gefitinib chemical structure of OIS, including abundant DDR foci formation, have been detected in a number of distinct benign neoplastic lesions

in humans and not in the corresponding malignant cancers [51, 52, 53 and 54••]. Given that initiation of aberrant cell proliferation in human tissues is often associated with oncogenic events, these data are strong evidence that OIS also suppresses cancer progression in humans. Some chromosomal loci, called common fragile sites (CFS), appear to be hot-spots for DSB formation as a result of DNA replication stress. These sites are usually repetitive in nature and have a tendency to form secondary structures that can impede replication fork progression [55]. In addition, CFS BGB324 order belong to chromosomal regions poor of replication origins and thus unable to cope with stalled DNA replication forks [56]. Because of their repetitive nature, sensitivity to oxidative damage, and propensity to form secondary structures (called G quadruplexes), telomeres also pose a challenge to the replication machinery. In fact, telomeres share many other features of CFS [57 and 58]. Not too surprisingly, therefore, recent results demonstrated

that oncogene expression leads to DNA replication stress, replication fork stalling, and formation of DDR foci at increased rates at telomeres [54••]. However, non-telomeric DDR foci are also generated but are resolved over a period

of several days in arrested oncogene-expressing cells. These telomeric DDR foci persist suggesting that also oncogene-induced telomeric lesions are not efficiently repaired. Does the persistence IKBKE of the telomeric DDR foci cause oncogene-expressing cells to arrest stably? In support of this, overexpression of catalytically active telomerase prevents formation of telomeric DDR foci as a result of oncogene-induced and drug-induced DNA replication stresses. Consequently, telomerase destabilizes the proliferative arrest caused by aberrant oncogene signalling [54••]. Thus, OIS is a cellular stress response that can be enforced by telomere dysfunction. Persistent telomeric DDR foci, or dysfunctional telomeres, can also be observed in most cells of benign human neoplasias and cancer precursor lesions before telomeres have become eroded. Foci form below a critical telomere length in most cells of benign human neoplasias and cancer precursor lesions such as melanocytic nevi, ductal breast hyperplasias, and colonic adenomas [54••]. Indeed, dysfunctional telomeres in cells comprising these benign lesions on average are not shorter compared to other telomeres in the same cells, supporting this conclusion.

Our previous studies demonstrated that EHop-016, at concentrations < 10 μM, inhibits the Rac activity of metastatic breast cancer cells MDA-MB-435 and MDA-MB-231 [52], as well as the SKBR3 cell line (data not shown). To determine the potential of EHop-016 as a general Rac inhibitor, we also tested the effect of EHop-016 in the metastatic prostate cancer cell line PC3; a cell line that has been shown to be dependent on Rac/Vav signaling for migration/invasion [67]. Figure 5A demonstrates that 8 μM EHop-016 inhibits the Rac activity of PC3 cells by 50%. To understand the mechanisms by which EHop-016 may reduce cell survival

and induce apoptosis, we investigated the effect of EHop-016 on known Rac/Cdc42/PAK signaling pathway molecules, which have been implicated in controlling cell survival and proliferation. Activated Rac and Cdc42 selleck may affect cell cycle progression via up-regulation JQ1 supplier of the oncogenes Cyclin D and c-Myc [10], [19], [68], [69] and [70]. Rac/PAK signaling also regulates cell growth via signaling to Akt, ERK, JNK, and p38 MAPK [16] and [71]. Figure 4 and Figure 5 show that in both MDA-MB-435 and PC3 cells, EHop-016 significantly reduced the expression of the oncogenic cell cycle regulators c-Myc and Cyclin D expression

by ~ 25% to 60%. Next, we investigated the effect of EHop-016 on MAPK activity and expression. EHop-016 did not affect ERK activity or expression (data not shown). However, EHop-016 significantly reduced the JNK activity of MDA-MB-435 cells by ~ 30%. In PC3 prostate cancer cells, p-JNK levels were decreased but total JNK levels were also reduced to a similar extent, indicating that JNK expression is also down-regulated in this cell line. Moreover, in the MDA-MB-435 cells, EHop-016 reduced Akt activity by 40% at 4 and 8 μM, without affecting

the Akt activity of PC3 cells (data not shown). These differences may be attributed to disparate cancer types of the two different cell lines. Studies have also linked Akt activity PRKACG and thus, the regulation of the anti-apoptotic protein BAD with Rac action [72], and may account of the observed reduction in caspase activity in the MDA-MB-435 cell line, where a parallel 1.4-fold calculated increase in caspase activity is observed at 8 μM, when Akt activity is decreased by − 1.4-fold (Figure 4, A and B). Therefore, EHop-016 may reduce cell viability and tumor growth via a number of Rac-regulated pathways that control cell survival and death. We have demonstrated that EHop-016 is a viable tool for blocking Rac activity via inhibition of the Vav/Rac interaction and thus, metastatic breast cancer cell migration In Vitro at μM concentrations [52]. Following this publication, the utility of EHop-016 as a Rac inhibitor has also been demonstrated in leukemia and melanoma cells [50] and [53].

The increase in the area of sea surface depends on the geometry of the surface waves. In order to estimate this increase in sea area we first discuss regular surface waves. Let us consider the ocean surface (without waves) in the form of a rectangle with dimensions a and b, where a lies parallel

to the x axis and b is parallel to the y axis. Panobinostat The area of the surface is therefore S0 = a × b. How will the area of this sea surface change when a regular wave of height H and length L propagates in the direction of the x axis? As the crest of a regular wave is parallel to the y axis, the sea surface elevation for a given time t = 0 is equation(71) ζ(x)=H2cos(2πxL).The area of a wind-roughened surface can therefore be given by equation(72) S=l b,S=l b,in which l is the length of the arc of the wave profile, when we intersect the Dasatinib manufacturer sea surface by a vertical plane parallel to the x axis within the limits from x = 0 to x = a. The length arc l becomes (Abramowitz & Stegun 1975) equation(73) l=∫0a1+(∂ζ(x)∂x)2dx.After substituting eq. (73) in eq. (72) we get equation(74) S=Lb2π∫0ka1+(kH2)2sin2(u) du,in which k is the wave number k = 2π/L. The exact solution

of equation (74) is expressed in the form of an elliptic integral of the second kind (Abramowitz & Stegun 1975), which cannot be obtained analytically. However, as the quantity kH/2 = πH/L is usually very small, we can expand the function under the integral into a Taylor series as follows: equation(75) 1+(kH2)2sin2u≈1+12(kH2)2sin2(u)−18(kH2)2sin4(u)+⋯As we are dealing with regular waves, we can

restrict ourselves to one wave length and thus take a = L (ka = 2π). Using this in eq. (74), we obtain equation(76) S=Lb[1+14(kH2)2−364(kH2)4+⋯].Therefore, the relative increase in the sea surface area becomes equation(77) δ=(S−S0)/S0=[14(kH2)2−364(kH2)4+ ⋯].The relative increase in sea surface area δ = (S – S0)/S0 (in %) as a function of wave steepness H/L is illustrated in Figure 6. Let us now assume that two regular surface waves of heights H1 and H2, and lengths L1 and L2 are propagating in two different directions θ1 and θ2. The resulting surface Amobarbital elevation takes the form equation(78) ζ(x, y, t)=H12cos[2πL1(x cosθ1+y sinθ1)−ω1t]++H22cos[2πL2(x cosθ2+y sinθ2)−ω2t],and the area of wave surface is now (Abramowitz & Stegun 1975) equation(79) S=∫0a∫0b1+(∂ζ∂x)2+(∂ζ∂y)2dy dx,in which a and b are the dimensions of a sea surface area without waves. Figure 7 presents the relative increase in sea surface area δ = (S – S0)/S0 as a function of the angle propagation difference(θ1 – θ2) for short waves (H1 = H2 = 1 m, T1 = T2 = 4 s). The maximum increase in sea area (about 6%) is observed for waves propagating in the same or in opposite directions.

56 CA titers typically range between 512 and 32000. DAT is always positive for C3d.[3] and [56] Most

reported patients have been adults, and AIHA typically occurs during the second or third week after the febrile illness has started.56 In most published cases the MK1775 onset has been sudden with pallor, jaundice and, sometimes, prostration. Intravascular hemolysis, as evidenced by hemoglobinuria, has been reported in several patients. In general, the prognosis is good and the hemolytic complication is self-remitting within 4–6 weeks, although a lethal course has been described in one patient.[55] and [56] A number of case reports have been published on CA mediated AIHA in infectious mononucleosis with confirmed Epstein–Barr virus (EBV) etiology.[57], [58], [59] and [60] As compared to M. pneumoniae pneumonia, however, infectious mononucleosis is an infrequent cause of AIHA, accounting for approximately 1% of the cases. [1] and [2] Conversely, the frequency of clinically significant hemolysis in EBV infections is unknown but probably low. Hospital-based data have indicated GSK J4 mouse that hematological complications, being generally mild and including several manifestations

other than AIHA, occur in 25–50% of patients with EBV infection. 59 Since patient selection will influence such figures and most individuals with infectious mononucleosis are not hospitalized, the frequency is probably much lower among patients with EBV-infection in the community. CA found in EBV-infections are polyclonal and almost invariably specific for the i-antigen.[57], [60] and [61] The immunoglobulin class may be either IgM or IgG.60 Rheumatoid factor-like IgM-IgG complexes have also been reported to act as CA in single cases.60 In most published reports, DAT has been positive for C3d only. Anti-i titers are usually modest, typically at 256–512, and the hemolytic anemia is transient and generally mild.60 Several authors have reported on transient CAS mediated

by anti-i autoantibodies following cytomegalovirus (CMV) infection.[60] and [61] Rarely, CA-mediated hemolysis has been described in adenovirus infections, influenza A, varicella, rubella, Legionella pneumophilica pneumonia, Resveratrol listeriosis and pneumonia caused by Chlamydia species. [11], [60], [62], [63], [64] and [65] We observed a slight, transient CAS in an otherwise healthy 23 year old man two weeks after a Chlamydia pneumoniae pneumonia. Severe CAS with a prolonged course and cryoglobulin activity of the CA has been reported following Escherichia coli lung infection. 22 Autoantibody specificities in these rare cases have included anti-I, anti-i and anti-Pr. Cold-antibody AIHA with infectious etiology typically involves a young adult or adolescent with M. pneumoniae pneumonia or infectious mononucleosis. Anemia or hemoglobinuria in such patients should immediately raise the suspicion of secondary AIHA.