Effects of Trichobilharzia ocellata on hemocytes of Lymnaea stagnalis

We analyzed the effects of infection with Trichobilharzia ocellata on hemocytes of its snail host, Lymnaea stagnalis, and correlated them with successive stages of parasite development. Circulating hemocytes were studied at 0, 2, 4, 6, and 8 weeks post exposure (p.e.) with respect to cell number, distribution of subpopulations (as characterized by morphology, determinants recognized by either of two lectins and a monoclonal antibody) and to proliferative, phagocytic and endogenous peroxidase activity. Infection results in a net elevated level of activity of circulating hemocytes at 2 weeks p.e., when mother sporocysts are present in the head-foot-mantle region, as well as at 4 weeks p.e., when daughter sporocysts are migrating to and growing in the digestive gland region. A lower level of activity was observed at 6 weeks p.e., when cercariae are differentiating within daughter sporocysts. A net activation was again found at 8 weeks p.e., when cercariae are escaping. So, infection with T. ocellata results in a net general activation of the internal defense system of L. stagnalis, during several stages of development of the parasite.     

Post-Vietnam stress disorder: a metaphor for current and past life events

Delayed posttraumatic stress reactions are often triggered by events that echo the original trauma. It is not uncommon, however, for these delayed reactions to represent a metaphor for other current or past life events. A case is presented that illustrates the diagnostic and therapeutic significance of understanding these reactions as a metaphor.     

Abnormalities of the first and second stages of labor

Abnormalities of the first and second stages of labor refer for the most part to abnormal progression of labor. This article discusses the risk factors, diagnoses, management options, and outcomes of the various categories of labor abnormalities, and provides an evidence-based approach where one exists. The article concentrates on the term, healthy woman carrying a singleton, vertex, normally grown fetus with no anomalies.     

Bacteriological profile of bacteremias in badly burnt patients

The purpose of this work is to study the bacteriological profiles of germ responsible for bacteriemas / septicemias in badly burnt patients hospitalized in burns utis, in order to guide better the antibiotherapy of first intention. During the period of survey going from January 1st, 2001 to December 31st,2002 71 patients had one or several episodes of bateremia. The average burnt cutaneous surface was 48.7%. All collected bacteriemas were contacted in hospial. Empirical antbiotheray was effective in 30 patients. The hospital stay for this group was long: 45 to 86 days. Acinetobacter baumannii was the most incriminated germ(20.3%), followed klebsiella pneumoniea (12.7%). The frequency of resistance was variable according to the considered species.     

Dynamic JUNQ inclusion bodies are asymmetrically inherited in mammalian cell lines through the asymmetric partitioning of vimentin

Aging is associated with the accumulation of several types of damage: in particular, damage to the proteome. Recent work points to a conserved replicative rejuvenation mechanism that works by preventing the inheritance of damaged and misfolded proteins by specific cells during division. Asymmetric inheritance of misfolded and aggregated proteins has been shown in bacteria and yeast, but relatively little evidence exists for a similar mechanism in mammalian cells. Here, we demonstrate, using long-term 4D imaging, that the vimentin intermediate filament establishes mitotic polarity in mammalian cell lines and mediates the asymmetric partitioning of damaged proteins. We show that mammalian JUNQ inclusion bodies containing soluble misfolded proteins are inherited asymmetrically, similarly to JUNQ quality-control inclusions observed in yeast. Mammalian IPOD-like inclusion bodies, meanwhile, are not always inherited by the same cell as the JUNQ. Our study suggests that the mammalian cytoskeleton and intermediate filaments provide the physical scaffold for asymmetric inheritance of dynamic quality-control JUNQ inclusions. Mammalian IPOD inclusions containing amyloidogenic proteins are not partitioned as effectively during mitosis as their counterparts in yeast. These findings provide a valuable mechanistic basis for studying the process of asymmetric inheritance in mammalian cells, including cells potentially undergoing polar divisions, such as differentiating stem cells and cancer cells.Aging is universally associated with a global decline in cellular function (1–3). Due to the multiplicity of mechanisms that undergo aging-related dysfunction, its mechanistic basis, or “senescence factor,” has been difficult to pinpoint. Several studies have provided key insight into the identities of senescence factors by studying the asymmetric segregation of damage in single-cell organisms that rejuvenate the emerging generation by preventing the inheritance of damaged factors such as DNA, lipids, and proteins (1, 4, 5). In particular, a number of seminal studies have demonstrated that bacteria and yeast use a complex and multifaceted machinery to prevent the inheritance of damaged and aggregated proteins by the new generation by restricting them to the older lineage during cell division (1, 6, 7).Although the precise mechanism for asymmetric inheritance of aggregates has been a matter of much debate (1, 7), the emerging model is that the spatial arrangement of misfolded proteins into quality control-associated IB (inclusion body)-like structures plays an essential role in asymmetric inheritance (1, 7). A key property of some quality-control IBs and other IB-like structures, which allows the cell to retain them in a specific lineage during mitosis, is their association and interaction with cellular organelles and cytoskeleton. In bacteria, for example, aggregated proteins are collected at the old pole of a dividing cell (5). A similar mechanism has been proposed in fission yeast (8). In the budding yeast Saccharomyces cerevisiae, several detailed studies demonstrated interdependence between asymmetric inheritance and the maintenance of the actin cytoskeleton and, in particular, the polarisome complex, which anchors the actin cytoskeleton in the emerging bud (9). Compromising the architecture of the actin cytoskeleton, even for a single generation, leads to a decrease in the replicative lifespan of the emerging cells (4).Yeast cells manage the triage of protein misfolding and aggregation by spatially partitioning subpopulations of misfolded proteins to several membrane-less cytosolic quality-control IBs (10, 11). Upon misfolding, substrates localize to transient stress foci (SFs), which concentrate chaperones, holdases, and disaggregases (7). SFs are dynamic IBs that form in response to acute stress and may participate in the triage decision of whether to refold, degrade, or aggregate misfolded proteins (7). As misfolded substrates accumulate, and especially in response to external stresses, they accumulate in two quality-control IBs: Proteins targeted for degradation are directed to the JUNQ compartment and proteins that are targeted for active aggregation are directed to an insoluble IPOD compartment (10). Recently, we have demonstrated a new vital role for these inclusions in asymmetric inheritance of aggregates (or spatial quality-control/replicative rejuvenation) in yeast (7). The IPOD and JUNQ are selectively retained in the mother cell during budding. This asymmetry is due to the fact that IPOD and JUNQ are tethered to organelles. Critically, proteins that were trapped in SFs, and therefore failed to migrate to IPOD or JUNQ in time for mitosis, were passed on to successive generations of daughter cells (7).Although a similar replicative rejuvenation mechanism in multicellular organisms has been sought after for some time, only a few seminal studies have found evidence for asymmetric aggregate segregation during mammalian or Drosophila mitosis (12, 13, 14). The mechanism for directing misfolded proteins to different inclusions structures, however, appears to be at least partially conserved from yeast to mammals. In previous work, we have demonstrated the existence of distinct IBs in human cultured cells: a JUNQ-like IB and an IPOD-like IB (from here on JUNQ and IPOD) (15, 16). The JUNQ contains mobile aggregates and accumulates chaperones, such as Hsp70, and active proteasomes (15). The IPOD sequesters insoluble amyloid aggregates from the rest of the cytosol (15). In striking similarity to the yeast JUNQ, the properties of the mammalian JUNQ are highly sensitive to stress. Under low-stress conditions, the JUNQ is a dynamic liquid phase compartment with high-degradation capacity (11, 17). Increased exposure to misfolding stress or localization of disease-associated proteins to the JUNQ instead of the IPOD leads to the maturation of the JUNQ into a less dynamic solid phase compartment, inhibiting degradation and eventually killing the cell (15, 18).We set out to examine the mechanism of mitotic inheritance of misfolded proteins and aggregates in mammalian cells. Using long-term 4D imaging (19), we demonstrate asymmetric inheritance of JUNQ IBs during mitosis. Although the IPOD, containing amyloidogenic proteins, is frequently inherited by the same cell as the JUNQ, it is sometimes misinherited. Similar to yeast, we observe SFs in mammalian cells, which fail to be retained asymmetrically. We show that the inheritance of the JUNQ is mediated by the association of the JUNQ with the cytoskeleton. The misfolded proteins in the JUNQ are confined by a network of vimentin intermediate filaments and sometimes also actin (20). Whereas in yeast the JUNQ and IPOD are both tethered to organelles, the mammalian IPOD does not appear to specifically associate with the cytoskeleton or the MTOC (Microtubule Organizing Center). Therefore, a critical difference between yeast and mammalian asymmetry mechanisms may be a reduced ability to maintain the partitioning of insoluble amyloid aggregates. Finally, we show that replicative rejuvenation may confer a slight fitness advantage, under certain conditions, on the daughter cell that fails to inherit a JUNQ. In addition to uncovering a novel replicative rejuvenation mechanism in higher eukaryotes, our study suggests that vimentin establishes an axis of mitotic polarity in mammalian cells.     

Maternal and perinatal outcome of eclampsia over a decade at a tertiary hospital in Kuwait

Aims: To determine maternal and perinatal outcome of eclampsia patients over a decade.

Methods: Analysis of case records of all eclampsia cases from January 2005 to December 2014.

Results: There were 30 cases of eclampsia. The most significant risk factors for developing pre-eclampsia are unbooked cases (97%), nulliparity, young age, marriage?≤4 months, history of pre-eclampsia in previous pregnancy, remarriage, preexisting diabetes mellitus, interval between pregnancies?≥10 years, positive family history. The incidence of eclampsia was 0.05%, antepartum eclampsia 15 (50%), intrapartum 6 (20%) and postpartum 9 (30%) with no maternal deaths, and 1 perinatal death. Perinatal mortality was 33.3/1000. 22 (73%) patients received magnesium sulphate (MgSO₄) and 8 patients (27%) received Diazepam, of which 1 had recurrence of convulsions. All 15 antepartum cases were delivered by cesarean section as were 2 intrapartum. 13 (43%) of women delivered vaginally. Only 6 (20%) patients were of low socio-economic status and were primary school educated. Severe maternal complications occurred in 8 (27%), with abruptio placentae being the most common 3 (38%).

Conclusions: Incidence of eclampsia was low, with no maternal deaths. MgSO4 was found to be highly effective. Lack of antenatal care is a major risk factor.     

Low-dose computed tomography via spatially adaptive Monte–Carlo reconstruction

Low-dose computed tomography (CT) reduces radiation exposure but decreases signal-to-noise ratio (SNR) and diagnostic capabilities. Noise compensation can improve SNR so low-dose CT can provide valuable information for diagnosis without risking patient radiation exposure. In this study, a novel noise-compensated CT reconstruction method that uses spatially adaptive Monte–Carlo sampling to produce noise-compensated reconstructions is investigated. By adapting to local noise statistics, a non-parametric estimation of the noise-free image is computed that successfully handles non-stationary noise found in low-dose CT images. Using phantom and real low-dose CT images, effective noise suppression is shown to be accomplished while maintaining structures and details.