Small colony variants constitute a slow-growing subpopulation of bacteria with distinctive phenotypic and pathogenic traits. Phenotypically, small colony variants have a slow growth rate, atypical colony morphology and unusual biochemical characteristics, making them a challenge for clinical microbiologists to identify. Clinically, small colony variants are better able to persist in mammalian cells and are less susceptible to antibiotics than their wild-type counterparts, and can cause latent or recurrent infections on emergence from the protective environment of the host cell. This review covered the phenotypic, genetic and clinical picture associated with small colony variants, with an emphasis on staphylococci, for which the greatest amount of information is available.

Small Colony Variants: a Pathogenic Form of Bacteria that Facilitates Persistent and Recurrent Infections

Porcine circovirus type 2 (PCV2) infections: clinical signs, pathology and laboratory diagnosis.

Publications Financial Statement pursuant to rule 154-ter paragraph 1 of Legislative Decree No. 58/1998 Annual Report Annual Report on Form 20-F for the Securities and Exchange Commission Fact Book (in Italian and English) Eni in 2011 (in English) Interim Consolidated Report as of June 30 pursuant to rule 154-ter paragraph 2 of Legislative Decree No. 58/1998 Corporate Governance Report pursuant to rule 123-bis of Legislative Decree No. 58/1998 (in Italian and English) Remuneration Report pursuant to rule 123-ter of Legislative Decree No. 58/1998 (in Italian and English)

Annual Report 2011 -個人別教育研究報告-

Respiratory disease in pigs is common in modern pork production worldwide and is often referred to as porcine respiratory disease complex (PRDC). PRDC is polymicrobial in nature, and results from infection with various combinations of primary and secondary respiratory pathogens. As a true multifactorial disease, environmental conditions, population size, management strategies and pig-specific factors such as age and genetics also play critical roles in the outcome of PRDC. While non-infectious factors are important in the initiation and outcome of cases of PRDC, the focus of this review is on infectious factors only. There are a variety of viral and bacterial pathogens commonly associated with PRDC including porcine reproductive and respiratory syndrome virus (PRRSV), swine influenza virus (SIV), porcine circovirus type 2 (PCV2), Mycoplasma hyopneumoniae (MHYO) and Pasteurella multocida (PMULT). The pathogenesis of viral respiratory disease is typically associated with destruction of the mucocilliary apparatus and with interference and decrease of the function of pulmonary alveolar and intravascular macrophages. Bacterial pathogens often contribute to PRDC by activation of inflammation via enhanced cytokine responses. With recent advancements in pathogen detection methods, the importance of polymicrobial disease has become more evident, and identification of interactions of pathogens and their mechanisms of disease potentiation has become a topic of great interest. For example, combined infection of pigs with typically low pathogenic organisms like PCV2 and MHYO results in severe respiratory disease. Although the body of knowledge has advanced substantially in the last 15 years, much more needs to be learned about the pathogenesis and best practices for control of swine respiratory disease outbreaks caused by concurrent infection of two or more pathogens. This review discusses the latest findings on polymicrobial respiratory disease in pigs.

Polymicrobial respiratory disease in pigs

Clinical signs and pathological features are still the corner-stones to suspect and diagnose overt disease associated with PCV2 infection. The clinico-pathological scope of this viral infection has been expanded over time. From the initial description of postweaning multisystemic wasting syndrome, some enteric, respiratory and reproductive disorders have been subsequently linked with PCV2. Porcine dermatitis and nephropathy syndrome, an immunocomplex disease, has also been associated with infection by this virus. All together, these conditions have been grouped under the name of porcine circovirus diseases (PCVD) or porcine circovirus associated diseases (PCVAD). The precise mechanisms by which a PCV2 infected pig develops a PCV2 subclinical infection or a clinical PCVD/PCVAD are still to be fully elucidated, but inferences based upon clinical, gross and histologic findings from field cases of disease have been useful to suggest the pathogenesis of this viral infection. The objective of the present review is to update the current knowledge on the clinical and pathological scope of PCV2 infections, as well as on their diagnosis. Moreover, a proposal on a unified PCVD/PCVAD terminology and clearly defined diagnostic criteria for these conditions are also given. © 2011 Elsevier B.V. All rights reserved.

Porcine circovirus type 2 (PCV2) infections: Clinical signs, pathology and laboratory diagnosis

STUDY QUESTION
Which substances and signal transduction pathways are potentially active downstream to the effect of FSH and LH in the regulation of human oocyte maturation in vivo?


SUMMARY ANSWER
The regulation of human oocyte maturation appears to be a multifactorial process in which several different signal transduction pathways are active.


WHAT IS KNOWN ALREADY
Many studies in animal species have provided insight into the mechanisms that govern the final maturation of oocytes. Currently, these studies have identified several different mechanisms downstream to the effects of FSH and LH. Some of the identified mechanisms include the regulation of cAMP/cGMP levels in oocytes involving C-type natriuretic peptide (CNP), effects of epidermal growth factor (EGF)-related peptides such as amphiregulin (AREG) and/or epiregulin (EREG), effect of TGF-β family members including growth differentiation factor 9 (GDF9) and morphogenetic protein 15 (BMP15), activins/inhibins, follicular fluid meiosis activating sterol (FF-MAS), the growth factor midkine (MDK), and several others. However, to what extent these pathways and mechanisms are active in humans in vivo is unknown.


STUDY DESIGN, SIZE, DURATION
This prospective cohort study included 50 women undergoing fertility treatment in a standard antagonist protocol at a university hospital affiliated fertility clinic in 2016-2018.


PARTICIPANTS/MATERIALS, SETTING, METHODS
We evaluated the substances and signalling pathways potentially affecting human oocyte maturation in follicular fluid (FF) and granulosa cells (GCs) collected at five time points during the final maturation of follicles. Using ELISA measurement and proteomic profiling of FF and whole genome gene expression in GC, the following substances and their signal transduction pathways were collectively evaluated: CNP, the EGF family, inhibin-A, inhibin-B, activins, FF-MAS, MDK, GDF9, and BMP15.


MAIN RESULTS AND THE ROLE OF CHANCE
All the evaluated substances and signal transduction pathways are potentially active in the regulation of human oocyte maturation in vivo except for GDF9/BMP15 signalling. In particular, AREG, inhibins, and MDK were significantly upregulated during the first 12-17 h after initiating the final maturation of follicles and were measured at significantly higher concentrations than previously reported. Additionally, the genes regulating FF-MAS synthesis and metabolism were significantly controlled in favour of accumulation during the first 12-17 h. In contrast, concentrations of CNP were low and did not change during the process of final maturation of follicles, and concentrations of GDF9 and BMP15 were much lower than reported in small antral follicles, suggesting a less pronounced influence from these substances.


LARGE SCALE DATA
None.


LIMITATIONS, REASONS FOR CAUTION
Although GC and cumulus cells have many similar features, it is a limitation of the current study that information for the corresponding cumulus cells is not available. However, we seldom recovered a cumulus-oocyte complex during the follicle aspiration from 0 to 32 h.


WIDER IMPLICATIONS OF THE FINDINGS
Delineating the mechanisms governing the regulation of human oocyte maturation in vivo advances the possibility of developing a platform for IVM that, as for most other mammalian species, results in healthy offspring with good efficacy. Mimicking the intrafollicular conditions during oocyte maturation in vivo in small culture droplets during IVM may enhance oocyte nuclear and cytoplasmic maturation. The primary outlook for such a method is, in the context of fertility preservation, to augment the chances of achieving biological children after a cancer treatment by subjecting oocytes from small antral follicles to IVM. Provided that aspiration of oocytes from small antral follicles in vivo can be developed with good efficacy, IVM may be applied to infertile patients on a larger scale and can provide a cheap alternative to conventional IVF treatment with ovarian stimulation. Successful IVM has the potential to change current established techniques for infertility treatment.


STUDY FUNDING/COMPETING INTEREST(S)
This research was supported by the University Hospital of Copenhagen, Rigshospitalet, the Independent Research Fund Denmark (grant number 0134-00448), and the Interregional EU-sponsored ReproUnion network. There are no conflicts of interest to be declared.

Susanne Elisabeth Pors

Papers

Regulation of human oocyte maturation in vivo during the final maturation of follicles.