Skilled birth attendance-lessons learnt

To reduce the horrific maternal mortality figures that we have globally especially in resource poor countries, there was a global commitment to reduce maternal mortality by three-quarters by 2015 using 1990 as a baseline. To measure the achievement of this goal, two indicators: maternal mortality ratio and proportion of births attended by skilled attendance were selected. To ensure skilled attendance at birth for all women, the international community set a target of 80% by 2005, 85% by 2010 and 90% coverage by 2015. However, in 2008 only 65.7% of all women were attended to by a skilled attendant during pregnancy, childbirth and immediately postpartum globally with some countries having less than 20% coverage. With the global human resource crisis, achieving this target is challenging but possible. This paper provides a narrative review of the literature on the skilled birth attendance strategy identifying key challenges and lessons learnt.     

Smoking and female infertility: a systematic review and meta-analysis

The high prevalence of smoking among women in their reproductive years continues to be a matter of concern. The negative effects of smoking on general health are well known, but smoking may also affect fertility. The objective of the present study was to perform a systematic review of the literature to determine whether there is an association between smoking and risk of infertility in women of reproductive age, and to assess the size of this effect. In the 12 studies used for this meta- analysis, the overall value of the odds ratio (OR) for risk of infertility in women smokers versus non-smokers was 1.60 [95% confidence interval (CI) 1.34-1.91]. Studies of subfertile women undergoing in-vitro fertilization (IVF) treatment also show a reduction in fecundity among women smokers. A meta-analysis of nine studies found an OR of 0.66 (95% CI 0.49-0.88) for pregnancies per number of IVF- treated cycles in smokers versus non-smokers. Despite the potential limitations of meta-analyses of observational studies, the evidence presented in this review is compelling because of the consistency of effect across different study designs, sample size and types of outcome. However, continued reassurance is needed that the calculated overall effect is not in fact due to confounding variables.      

Differential coupling of CC chemokine receptors to multiple heterotrimeric G proteins in human interleukin-2-activated natural killer cells

Using two different approaches, we have investigated the types of G proteins coupled to CC chemokine receptors. First, permeabilization of interleukin-2-activated natural killer (IANK) cells with streptolysin-O and introduction of anti-G protein antibodies inside these cells resulted in the following. (1) Anti-G(s), anti-G(o), and anti-G(z) inhibited the migration of IANK cells in response to macrophage- inflammatory protein-1 alpha (MIP-1 alpha), monocyte chemoattractant protein-1 (MCP-1), or regulated on activation normal T cell expressed and secreted (RANTES). (2) Anti-Gi inhibited their migration in response to MCP-1 or RANTES but not in response to MIP-1 alpha. Second, incubation of IANK cell membranes with anti-G protein antibodies before incubating with (gamma-35S) GTP or (gamma-32P) GTP, resulted in the following. (1) Anti-G(s), anti-G(o), or anti-G(z) inhibited GTP binding and GTPase activity in the presence of MIP-1 alpha, or RANTES. (2) Anti- G(i) inhibited GTP binding and GTPase activity in the presence of MCP-1 or RANTES but not in the presence of MIP-1 alpha. The inhibitory effect of anti-G protein antibodies was reversed upon incubating these antibodies with their respective synthetic peptides before addition to IANK cell membranes. These results suggest that MCP-1 and RANTES receptors are promiscuously coupled to multiple G proteins in IANK cell membranes and that this coupling is different from MIP-1 alpha receptors, which seem to be coupled to G(s), G(o), and G(z) but not to G(i).     

Pre-B acute lymphoblastic leukemia cells may induce T-cell anergy to alloantigen

Even if neoplastic cells express tumor associated antigens they still may fail to function as antigen presenting cells (APC) if they lack expression of one or more molecules critical for the induction of productive immunity. These cellular defects can be repaired by physiologic activation, transfection, or fusion of tumor cells with professional APC. Although such defects can be repaired, antitumor specific T cells may still fail to respond in vivo if they may have been tolerized. Here, human pre-B cell acute lymphoblastic leukemia (pre-B ALL) was used as a model to determine if primary human tumor cells can function as alloantigen presenting cells (alloAPC) or alternatively whether they induce anergy. In the present report, we show that pre-B cell ALL express alloantigen and adhesion molecules but uniformly lack B7-1 (CD80) and only a subset express B7-2 (CD86). Pre-B ALL cells are inefficient or ineffective alloAPC and those cases that lack expression of B7-1 and B7-2 also induce alloantigen specific T- cell unresponsiveness. Under these circumstances, T-cell unresponsiveness could be prevented by physiologic activation of tumor cells via CD40, cross-linking CD28, or signaling through the common gamma chain of the interleukin-2 receptor on T cells. Taken together, these results suggest that pre-B ALL may be incapable of inducing clinically significant T-cell-mediated antileukemia responses. This defect may be not only due to their inability to function as APC, but also due to their potential to induce tolerance. Attempts to induce clinically significant antitumor immune responses may then require not only mechanisms to repair the antigen presenting capacity of the tumor cells, but also reversal of tolerance.     

Selection bias: neighbourhood controls and controls selected from those presenting to a Health Unit in a case control study of efficacy of BCG revaccination

Background  

In most case control studies the hardest decision is the choice of the control group, as in the ideal control group the proportion exposed is the same as in the population that produced the cases.     

Laparoscopic hysterectomy in a case of male pseudohermaphroditism with persistent Mullerian duct derivatives

We describe laparoscopic diagnosis and treatment for a case of dysgenetic male pseudohermaphroditism with persistent Mullerian ducts. The patient, a 32 year old man, with a history of surgery for hypospadias and cryptorchidism during childhood, was referred because of anejaculation. He was of short stature, with male external genitalia composed of a small penis and hypoplastic testis (1 ml right, 6 ml left side). Plasma follicle stimulating hormone (FSH) was high (17 mUI/ml), testosterone low (1.9 ng/ml), and his karyotype was 46,XY. Pelvic ultrasound, nuclear magnetic resonance (NMR) and genitography disclosed a uterine-like structure with cavity communicating with the urethra. Laparoscopy and urethrocystoscopy confirmed the presence of a 4 cm uterus, which was removed endoscopically at the same time. A biopsy of the left gonad was also performed. The uterus contained endometrial tissue and was fibrotic. Histology of the left gonad showed spermatocytic arrest. We diagnosed dysgenetic male pseudohermaphroditism. Laparoscopy, in our opinion, is an optimal tool to diagnose and treat abnormal sexual conditions.