The opening chapter is key in attempting to teach the reader, rather than requiring the reader to read and understand. For me, this leads to a deeper level of learning, and therefore I think the book is particularly valuable for neuropathologists in training and histopathologists who are interested in neuropathology. The editors have a self-professed commitment to education and are internationally renowned neuropathologists, and the generosity of knowledge in this book is clear. There are 28 contributors, from the USA, Canada, France, PKC412 order Germany and Portugal. The entire book is very well illustrated, with large good-quality colour images of

macroscopic findings, histology, immunohistochemistry and radiology. Images are also included of important molecular tests, for example, dual-colour fluorescence in situ hybridization, and there are a few electron microscopy images. Coloured headers and footers relating to chapter identity are a nice touch. There are several useful tables, again with colour coding that makes interaction with the book very easy. The index, learn more at nearly 50 pages long, is as comprehensive as the book itself. It is printed on good-quality paper, and hard bound. As part of the expert consult

series, the book comes with access through registration at http://www.expertconsult.com to a wealth of images, which may be downloaded and imported into PowerPoint presentations. After the opening ‘pattern’ chapter there is a good description of normal (primarily adult) brain histology, followed by equally useful descriptions of common surgical artefacts and pragmatic intraoperative basics. A fourth chapter explains common and advanced neuroradiological techniques, with well-illustrated examples, and a whole-page table of relevant patterns. Approximately Docetaxel half of the book is dedicated to tumour

pathology. There are 13 tumour chapters, including one each on peripheral nerve sheath tumours, lymphomas and histiocytic tumours, germ cell tumours, melanocytic neoplasms and pituitary pathology. Following this, there are good chapters on iatrogenic disease, familial tumour syndromes, then inflammatory conditions, white matter disease, epilepsy, vascular disorders and the biopsy in neurodegenerative disorders. If I am to find criticisms, they are minor. With such a useable, practical book, I would have preferred a soft cover to keep the relevant page propped open on my desk. There is no nerve, muscle, bone or ophthalmic section. With the surgical nature of this book, these absences are excusable and understandable, but I cannot help feeling the authors would have benefitted their readers by including their take on broader neuropathological specimens. The preface refers to neuropathology songs used by one of the editors – I have yet to sample these, but will do so quietly, in my office, with the door shut.

But will any single biomarker such as NGAL suffice in AKI? In addition to early diagnosis and prediction, it would be desirable to identify biomarkers capable of discerning find more AKI subtypes, identifying aetiologies, predicting clinical outcomes, allowing for risk stratification and monitoring the response to interventions. In order to obtain all of this desired information, a panel of validated biomarkers may be needed. Other AKI biomarker

candidates may include interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), cystatin C and liver-type fatty acid binding protein (L-FABP), to name a few.1–3 The availability of a panel of validated AKI biomarkers, such as those illustrated in Figure 1, could further revolutionize and personalize renal and critical care in the near future. Studies cited in this review that were performed by the author’s laboratory were supported by grants from the NIH (R01 DK53289, RO1 DK069749 and R21 DK070163). Dr Devarajan is a co-inventor on NGAL patents. Biosite(R) Incorporated has signed an exclusive licensing agreement with Cincinnati Children’s Hospital for developing plasma NGAL as a selleck biomarker of acute renal failure. Abbott Diagnostics has signed

an exclusive licensing agreement with Cincinnati Children’s Hospital for developing urine NGAL as a biomarker of acute renal failure. Dr Devarajan has received honoraria for speaking assignments from Biosite(R) Incorporated and Abbott Diagnostics. “
“Date written: June 2008 Final submission: June 2009 Kidney transplant recipients should be advised to take a vitamin D (or analogue) supplement at a dose of at least 0.25 µg daily. (Level I and II) (Suggestions are based on Level III and IV evidence) The treating physician should determine the dose of vitamin D and the necessity of other treatments for minimizing bone mineral density loss, on the basis of available evidence. A rapid decline in bone mineral density occurs in the early post-transplant period.3,4 Though the rate of bone loss may decelerate or cease by around 3 years post-transplant, bone mineral ADP ribosylation factor density remains below normal.5 The risk of bone fractures

among kidney transplant recipients is four times that among the general population.6 At the time of transplantation, there are usually already significant abnormalities of bone remodelling related to chronic kidney disease.7 Reduced calcium absorption due to prednisone,8 hyperparathyroidism9 and abnormal vitamin D metabolism10 are among the factors contributing to the further weakening of bones and the risk of bone disease post-transplantation. There is an increased risk of bone loss among females, particularly post-menopausal.11 This review set out to explore and collate the evidence to support the use of particular nutrition interventions for the prevention and management of bone disease in kidney transplant recipients, based on the best evidence up to and including September 2006.

The link between Tregs and the ‘hygiene hypothesis’ is discussed in detail elsewhere in this workshop. In principle, stimulation of the T cell system via microbial-derived signals selleck chemicals emanating principally from the GIT may be one route via which functionally mature Tregs are generated, and these cells may contribute to maintenance of homeostasis in peripheral tissues distal to the GIT. In early life, one source of such Tregs may be recent thymic emigrant (RTE) CD4+ T cells. Human in vitro studies from

our group and others [16,45,47], echoing earlier work in the mouse [48], have demonstrated that naive RTE which dominate the circulating CD4+ T cell compartment during infancy respond ‘non-specifically’ to peptides, leading to rapid activation and cytokine production which is usually terminated soon thereafter by apoptotic death. However, a subset of these RTE survive and potentially may thus enter the recirculating T cell compartment [16,47]. These survivors acquire Treg Selleckchem Luminespib activity during the activation process [16]; this process may reflect events occurring in the lymphoid drainage of the GIT under the influence of microbial-derived antigens, providing a continuous ‘drip-feed’ of functionally activated Tregs. The de novo generation

and/or boosting of existing Treg activity by controlled microbial stimulation of the GIT is one of the aims of probiotic therapies which are being tested in many centres internationally, but there are few direct data available to confirm the efficient operation of this mechanism in humans. However, recent mouse data support the potential feasibility of this approach. In particular, gavage of mice with a bolus of live Lactobacillus reuteri increases numbers and functional activity of

Tregs in central lymphoid organs [49]. Moreover, if this is carried out in sensitized animals prior to aeroallergen challenge, ensuing lung eosinophilia and airways hyperresponsiveness is attenuated significantly and this effect can Isotretinoin be reproduced by adoptive transfer of Tregs harvested from spleens of L. reuteri-gavaged animals [49]. We have obtained similar findings in a rat atopic asthma model employing repeated feeding with a microbial extract containing multiple TLR ligands, and moreover we have observed that the attenuation of aeroallergen-induced airways inflammatory responses in prefed animals is associated with increased baseline numbers of Tregs in the airway mucosa (to be published). These latter findings suggest that one of the principle tenets of the ‘common mucosal immune system’ concept, notably that adaptive immune cell populations activated in the GIT mucosa will subsequently traffic preferentially to other mucosal sites, may be exploitable in relation to therapeutic control of allergy-induced lung inflammation.

It is important that only studies matching the inclusion criteria are included in the systematic review, so that the systematic review answers a specific clinical question. Prospective criteria for study inclusion and exclusion should be explicitly SCH727965 mouse stated in the review to minimize selectivity by authors. These criteria are a requirement before commencing Cochrane reviews, when a study protocol is developed, peer reviewed and published before initiating the review. The decision regarding which studies to include in a systematic review may have an important effect on a conclusion, say regarding the overall utility

of a healthcare intervention.13 Therefore, study inclusion assessment should be completed independently by at least two authors and generally is arbitrated by a third. Readers of systematic reviews can look for a flow chart (usually presented as a Fig. 1) describing the details of studies identified, studies excluded, reasons for exclusion and numbers of studies included in the final review. If the outcome of interest is dichotomous (the outcome

is one of two possibilities – example, death or survival) the treatment effect is calculated for each trial as a risk ratio, an odds ratio or a risk difference together with the 95% confidence interval (95% CI; the range Obeticholic Acid research buy within which we are 95% confident that the effect calculated is likely to exist). While full discussion of all methods Methane monooxygenase is beyond the scope of this review, dichotomous outcomes are frequently evaluated as a relative risk (RR), which deserves a brief explanation. A RR divides the event rate in the intervention group (number of events divided by the total number of individuals randomized in that group) by the event rate in the comparison group. For example, if 20 of 100 patients in the active intervention group who are randomized to

erythropoietin to normalize haemoglobin levels experienced an event and 10 of 100 patients in the control group (those randomized to a lower haemoglobin target), experienced the event, then the RR is 2 (20/100 divided by 10/100), indicating that the intervention is twice more likely than the comparison treatment to result in the outcome. Interpretation of this risk for the specific patient is possible when the actual risk of the outcome for that patient without treatment is known (e.g. when RR = 2, a doubling of risk from 2% to 4% is quite different from the doubling of risk from 10% to 20% in the present example). If the outcome of interest is a continuous variable (an example is systolic blood pressure, mmHg), then the effect size of the intervention is summarized as a mean difference (MD; and its 95% CI). The MD for the outcome in each trial is the amount by which an intervention changes the outcome on average compared with the control.

The total median BVAS/WG score in these patients was 5 (IQR 3–8), and median BVAS/WG score calculated for eye and airway involvement was 3 (2.8–5.5) (Fig. 1). The frequency of disease distribution and BVAS/WG scores are shown in Table S2. At 6 months, a significant decrease was Inhibitor Library observed in BVAS ENT-EYE-L score [medians before 3 (3–6) versus 2 (1–3), P = 0.02]. Five patients (29%) had a ≥50% treatment response regarding the ENT-EYE-L

manifestations including 1 patient with complete remission. Ophthalmic manifestations, confirmed by MRT in three patients, improved clinically in two patients and progressed in one patient. No clinical improvement was seen in three patients with endobronchial disease in response to RTX treatment (Fig. 4). One patient with tracheal-subglottic stenosis improved clinically, whereas no treatment response was seen in the second selleck patient and progression was observed in the third patient. Multiple nodules and cavities in the lungs diagnosed in five patients resolved in four cases within 5–8 months after RTX treatment initiation, and in one patient, a significant improvement was seen (Fig. 5). For more detailed descriptions, see Supporting information. Rituximab was generally well tolerated, and no serious infusion reactions were observed. No deaths occurred during the follow-up period. However, eight patients (28%)

experienced severe life-threatening events or required hospitalization during the follow-up period because of severe infections. Two patients (7%) needed additional medications owing to pulmonary Pneumocystis jiroveci infections, and one had a severe Aspergillus pneumonia infection. One patient had a severe Herpes infection with Pregnenolone signs of meningitis that was successfully treated with acyclovir. Three patients (10%) developed severe neutropenia, whereas one of them displayed generalized bone marrow suppression. Although these three patients received high doses

of oral CYC also, the additive effect of RTX should be considered. During the follow-up period, one patient was diagnosed as having breast cancer. Another patient with a severe relapsing disease (duration more than 27 years) and multiorgan involvement was hospitalized three times during follow-up period owing to erysipelas, sepsis and septic arthritis. This patient had previously been diagnosed as having a urinary bladder cancer 3 years before RTX treatment. One patient suffered haemorrhagic cystitis, a common complication of CYC treatment. The current standard therapy for ANCA-associated vasculitis is high-dose steroids and CYC, the latter being associated with severe adverse events such as leucopoenia, cancers, severe infections, gonadal failure and premature menopause in women. Although it is effective in approximately 80% of patients [17], there is an unmet need for more efficient and less toxic therapies in these patients.

Cell viability was determined by Trypan blue exclusion in human acute monocytic leukaemia cell line (THP-1) cells treated for 24 h with different concentrations of tumour necrosis factor (TNF)-α and/or interferon (IFN)-γ as indicated. Grey bars correspond to the cytokine concentration selected for further studies; TNF-α (10 ng/ml) and IFN-γ (200 UI/ml). Fig. S3. Kinetic of transglutaminase

2 (TG2) induction by tumour necrosis factor (TNF)α + interferon (IFN)-γ. Caco-2 and human acute monocytic leukaemia cell line (THP-1) cells were incubated for different times with TNF-α (10 ng/ml) and IFN-γ (200 UI/ml). Levels of TG2 transcript were determined by quantitative real time–polymerase chain reaction (RT–PCR). Results were normalized against β-actin and relative TG2 mRNA levels were referred to the non-stimulated control (value = 1). Data represent means ± standard error of the mean (n = 3). The Mann–Whitney U-test www.selleckchem.com/products/ganetespib-sta-9090.html was performed: *P < 0·05; **P < 0·01. "
“Citation Sater MS, Finan RR, Al-Hammad SA, Mohammed FA, Issa AA, Almawi WY. High frequency of anti-protein Z IgM and IgG autoantibodies in women with idiopathic recurrent spontaneous miscarriage. Am J Reprod Immunol 2011; 65: 526–531 Problem  Protein Z (PZ) system is an anticoagulant pathway learn more involved in the physiologic regulation of coagulation, and PZ deficiency reportedly enhances prothrombophilic mechanisms, including those

implicated with idiopathic recurrent miscarriage (RSM). We investigate plasma anti-PZ IgM and IgG levels in RSM women and in multiparous control women. Methods  Anti-PZ IgM and IgG levels were measured in 265 RSM women and 283 age-matched control women by ELISA. Results  Elevated anti-PZ IgG (P < 0.001) and IgM (P < 0.001) titers were seen in patients. The areas under the curves for ROC curve for anti-PZ IgM (0.898 ± 0.044) and IgG (0.898 ± 0.042) demonstrated no variation in diagnostic capacity. Casein kinase 1 Multivariate analysis confirmed the association of elevated anti-PZ IgM [adjusted odds ratio, aOR (95% CI) = 6.46 (2.44–17.11)] and IgG [aOR (95% CI) = 7.44 (2.54–21.79)] as independent predictors of RSM after adjusting for confounding covariates and demonstrated a clear gradation of increasing RSM risk associated with

increased antibody titers. Conclusion  The presence of anti-PZ IgM and IgG antibodies are risk factors for RSM. “
“Ifng/Ifngr1 are the main genes that are associated with tuberculosis. We continued to search for other functional single nucleotide polymorphisms (SNP) and investigated their influence on patients with tuberculosis in the Chinese population. Seven SNP located in the ifng and ifngr1 genes were genotyped by ligase detection reaction in 222 cases and 188 ethnically matched controls. A significant genetic association between rs7749390 (located on the exon/intron splice site of the ifngr1 gene) and tuberculosis was observed, and the log-additive model was accepted as the best inheritance model to fit these data (OR: 1.35, 95% CI: 1.02–1.80, P = 0.038).

We thank Ministerio de Educación y Ciencia and FECYT (Spain) for a postdoctoral fellowship to O. Palomares. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“Citation Rosenberg VA, Buhimschi IA, Dulay AT, Abdel-Razeq SS, Oliver EA, Duzyj CM, Lipkind H, Pettker CM, Buhimschi CS. Modulation of amniotic fluid activin-A and inhibin-A in women with preterm premature rupture of the membranes and infection-induced preterm birth. Am J Reprod Immunol 2012; 67: 122–131 Problem  Activins and inhibins are important modulators of inflammatory processes. We explored activation of amniotic fluid (AF) activin-A and inhibin-A system in women with intra-amniotic

infection and preterm

premature rupture of the membranes (PPROM). Method of study  We analyzed 78 AF samples: ‘2nd trimester-control’ (n = 12), ‘3rd trimester-control’ Idasanutlin nmr (n = 14), preterm labor with intact membranes [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)], and PPROM [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)]. Activin-A levels were evaluated ex-vivo following incubation of amniochorion and placental villous explants with Gram-negative lipopolysaccharide (LPS) or Gram-positive (Pam3Cys) bacterial mimics. Ability of recombinant activin-A and inhibin-A to modulate inflammatory reactions in fetal membranes was explored through explants’ IL-8 release. Selleck Bortezomib Results  Activin-A and inhibin-A were present in human AF and were gestational age-regulated. Activin-A

was significantly upregulated by infection. Lower inhibin-A levels were seen in PPROM. LPS elicited release of activin-A from amniochorion, but not from villous explants. Recombinant activin-A stimulated IL-8 release from amniochorion, an effect that was not reversed by inhibin-A. Conclusion  Human AF activin-A and inhibin-A are involved in biological processes linked to intra-amniotic infection/inflammation-induced PRKD3 preterm birth. “
“National Institute for Medical Research, London, UK Cancer Research UK London Research Institute, London, UK The early growth response (Egr) transcription factor family regulates multiple steps during T-cell development. We examine here the role played by Egr2 in positive selection. In double-positive cells, Egr2 is upregulated immediately following TCR ligation, and its expression requires both the MAPK and calcineurin signaling pathways. Inducible transgenic and knockout mice were generated to cause gain- or loss-of-function of Egr2 in double-positive cells, and had reciprocal effects; more mature single-positive cells were made when Egr2 was overexpressed, and fewer when Egr2 was absent. These defects were associated with changes in the survival of positively selected cells rather than perturbation of positive selection or immediate post-selection signaling.

© 2010 Wiley-Liss, Inc. Microsurgery 30:339–347, 2010. “
“Lymphaticovenular anastomosis (LVA) is a useful treatment for compression-refractory lymphedema with its effectiveness and minimal invasiveness. However, LVA requires supermicrosurgery, where lymphatic vessels with a diameter of 0.5 mm or smaller are anastomosed using 11-0 or 12-0 suture. To make LVA easier and safer, we adopted a modified side-to-end (S-E) anastomosis in LVA surgery. We performed modified S-E LVAs in 14 limbs Romidepsin solubility dmso of female patients with lower extremity

lymphedema (LEL). In modified S-E LVA, lateral windows with a length of 1.0 mm or longer were created on a lymphatic vessel and a vein, respectively, and side-to-side (S-S) anastomosis was established with 10-0 continuous suture. After completion of S-S anastomosis, the vein distal to the anastomosis site was ligated to prevent venous backflow and subsequent thrombosis at the anastomosis site. Lymphedematous volume was evaluated preoperatively and at postoperative 6 months using LEL index. All the 24 modified S-E anastomoses could be completed without

difficulty or revision for anastomosis, and showed good patency after completion of anastomosis. Postoperatively, LEL indices significantly decreased compared with preoperative LEL index (255.9 ± 14.1 vs. 274.9 ± 22.2, P < 0.001). Modified S-E LVA can efficaciously divert lymph flows into venous circulation without performing supermicrosurgical anastomosis. © 2012 Wiley Periodicals, Inc., Microsurgery, 2013. "
“Functional reconstruction of the anterior mandibular Protirelin defect in combination Selleckchem Temsirolimus with a significant glossectomy is a challenging problem for reconstructive micro-surgeons. In this retrospective study, clinical results were compared between mandibular reconstruction plate (MRP) procedures and double flap transfers. The subjects were 23 patients who underwent immediate reconstruction, after an anterior segmental mandibulectomy in combination with a significant glossectomy, from 1993 to 2009. The patients were

divided into two groups based on the reconstructive methods used: MRP and soft tissue free flap transfer (MRP group: 12 patients) or double free flap transfer (double flap group: 11 patients). Operative stress, postoperative complications and oral intake ability were compared between the groups. The rate of recipient-site complication in the double flap group tended to be lower than that in the MRP group. The most frequent complications in the MRP group included infection and orocutaneous fistula. Operative stresses (operation time and blood loss) were significantly less in the MRP group than in the double flap group. Overall, 19 patients (82.6%) were able to tolerate an oral diet without the need for tube feeding. This study demonstrates that laryngeal preservation is possible in more than 80% of patients even after such an extensive ablation.

Mammalian pregnancy is a physiological transitory state of immune tolerance to the fetus that still remains incompletely understood.1,2 The maternal immune system is aware of the presence of the fetal semiallograft, but does not reject it. Several immune mechanisms are involved in the establishment of the active multifactorial maternal-fetal tolerance2: deviation of the systemic maternal immune system toward Th2 type of immune responses,3 expression of the non-classical HLA-G molecules by trophoblasts thus inhibiting maternal NK cell attack,4 promoting apoptosis of activated Fas+ maternal lymphocytes through

FasL expression by the syncytiotrophoblast,5,6 down-regulation of NKG2D receptor on maternal buy INK 128 peripheral blood mononuclear cells (PBMC) by placental exosomes carrying

NKG2D ligands7–9 and indoleamine 2,3-dioxidase-mediated tryptophan degradation that suppresses the immune response by inhibition of T- lymphocyte proliferation.10 The recently ‘rediscovered’ regulatory T cells (Treg cells) have emerged as key players in the control of the maternal immune Roxadustat cell line responses that could threaten the fetal semiallograft.11 Among the heterogeneous population of cells with regulatory function,12–14 two Treg subsets with the phenotype of CD4+ CD25+ stand out and comprise the vast majority: the naturally occurring/innate thymus-derived Treg cells and the inducible/adaptive Treg cells that can be generated in the periphery.15 Recent reports

have shown that these two cell populations of CD4+ CD25+ Treg cells, classified according to origin and generation, can acquire the same phenotypic markers and functional properties and be indistinguishable from each other.16,17 In each of these populations of Treg cells, sustained expression of the transcriptional repressor factor of the forked head/winged-helix family, known as Forkhead box P3 (Foxp3), is essential for Treg commitment, phenotype development, and immunosuppressive function.18–20 Recent studies have shown that Foxp3 acts as a quantitative regulator and can also be acquired by induced Treg cells in the periphery. Thus, high and stable Foxp3 expression is a marker for the Treg cell lineage albeit transient, low-level Foxp3 expression can occur in effector T cells.18–20 The Foxp3-dependent transcriptional program ZD1839 in vitro induces expression of CD25, cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), CD103, Neuropilin-1, LAG-3, and CD62L molecules that comprise the Treg phenotype and are closely associated with the CD4+ CD25+ Treg cell function. Contact-mediated suppression, characteristic for the Foxp3 expressing Treg cells, results from ligation of CTLA-4, membrane-bound TGFβ and LAG-3.14,21 Treg cells are also classified by their cytokine profile into Tr1 type, producing IL-10 and Th3 type, producing TGFβ.22 A key role for CD4+ CD25+ Treg cells during early pregnancy has been suggested both in humans and mice.

A total of 141 S. pyogenes strains belonging to 21 emm genotypes were analyzed. These included 138 strains obtained from patients with uncomplicated S. pyogenes infections, selleck chemical two strains isolated from patients with STSS, and one strain isolated from a sepsis patient. All strains were isolated between 1994 and 2006 in Toyama or Aichi Prefecture, Japan. emm genotypes were determined for all 141 strains according to the emm genotyping protocol (http://www.cdc.gov/ncidod/biotech/strep/strepindex.html). S. pyogenes SF370 (12) was included in all

examinations. A nonpolar inactivated mutant of the emm1 gene (SF370 Δemm1) was constructed in the chromosome of S. pyogenes SF370 through double-crossover allelic replacement. DNA fragments of emm1 were learn more amplified with the oligonucleotide primers emm-n5Nhe and emm-c4Sma (fragment 1) and emm-n6Sma and emm-c5Spe (fragment 2). The primers used in this study are shown in Table 1. NheI/SmaI-digested fragment 1 was inserted in the same site in pFW12 (13). The resultant plasmid was digested with SmaI and SpeI, and both SmaI/SpeI-digested fragment

2 and an spc2 DNA fragment containing aad9 (promoterless spectinomycin resistance gene) obtained from an SmaI-digested fragment of pSL60-2 (13) were inserted. This plasmid (emm1::aad9/pFW12) was a suicide vector for S. pyogenes. For the preparation of competent cells, strain SF370 was harvested at early- to mid-log phase (OD660 = 0.4–0.5) and washed twice with 0.5 M sucrose buffer. The constructed suicide vector was transformed into the strain by electroporation, which was conducted at 1.25 kV/mm, 25 μF capacitance, and 200 ohms resistance using a Gene Pulser II (Bio-Rad Laboratories, Hercules, CA, USA). After incubation at 37°C for 3 hr, competent cells were spread onto BHIY on agar plates containing spectinomycin (final concentration, 100 μg/mL). Selected colonies on the plates were cultured. Cultured bacteria were washed once with saline, resuspended in 10 mM Tris–1 mM EDTA, and boiled for 10 Cell press min. Genomic DNA was obtained from

the supernatant of boiled bacteria. Double-crossover replacement with genomic DNA was analyzed by PCR. Successful double-crossover replacement was further confirmed by DNA sequencing. SF370 ΔcsrS was prepared according to a previously described method (14). The M protein-high producer of emm1 was complemented with the csrS (I333V) gene. One of our previous studies had demonstrated that, judging from the exoprotein production profile, the csrS (I333V) gene cannot be functionally distinguished from the wild type gene (15). Preparation of the csrS-complemented strain has been described previously (15). A homology search of four different emm genes (emm1, 3, 6, and 12) revealed that a fragment of 360 bps between the C2 and D repeat regions (amino acid position: 286–405 referenced to the SF370 genome strain) was identical in these genes.