Providing skilled birth attendants and emergency obstetric care to the poor through partnership with private sector obstetricians in Gujarat, India

Problem

India has the world’s largest number of maternal deaths estimated at 117 000 per year. Past efforts to provide skilled birth attendants and emergency obstetric care in rural areas have not succeeded because obstetricians are not willing to be posted in government hospitals at subdistrict level.

Approach

We have documented an innovative public–private partnership scheme between the Government of Gujarat, in India, and private obstetricians practising in rural areas to provide delivery care to poor women.

Local setting

In April 2007, the majority of poor women delivered their babies at home without skilled care.

Relevant changes

More than 800 obstetricians joined the scheme and more than 176 000 poor women delivered in private facilities. We estimate that the coverage of deliveries among poor women under the scheme increased from 27% to 53% between April and October 2007. The programme is considered very successful and shows that these types of social health insurance programmes can be managed by the state health department without help from any insurance company or international donor.

Lessons learned

At least in some areas of India, it is possible to develop large-scale partnerships with the private sector to provide skilled birth attendants and emergency obstetric care to poor women at a relatively small cost. Poor women will take up the benefit of skilled delivery care rapidly, if they do not have to pay for it.     

消旋15(R)-15-甲基PGE2甲酯的合成

d,l-15(R)-15-Methyl-PGF_2α methyl ester 11-trimethylsilyl ether(II)wasprepared from selective monosilylation of d,l-15(R)-15-methyl-PGF_2αmethyl ester(I) withtrimethylsilyldiethylamine in acetone. Oxidation of(II ) with Collin's reagent gave d,l-15(R)-15-methyl-PGE₂ methyl ester 11-trimethylsilyl ether(III)which,without purification,was converted to d,l-15(R)-15-methyl-PGE₂ methyl ester(IV)under mild acidic conditions.     

用细口径反相柱HPLC分离多种前列腺素

HPLC与放射性同位素联用,可同时分离鉴定多种花生四烯酸代谢产物。目前国外一般是使用普通口径(4.6 mm)的反相柱,以30%左右乙腈为流动相,流速为1～3 ml/min。这种HPLC方法乙腈用量较大,费用太贵,不适合国内实验室常规操作。据报道,细口径     

Wallerian degeneration in a patient with Schilder disease: MR imaging demonstration

Wallerian degeneration in the corticospinal tract was demonstrated by magnetic resonance (MR) imaging in a patient with Schilder disease. The histochemical stages of myelin breakdown that allow its demonstration by MR imaging are reviewed.     

Swan-Ganz catheter-induced pulmonary artery pseudoaneurysm formation: three case reports and a review of the literature.

The use of Swan-Ganz catheters has increased tremendously since they were first introduced in 1970. Their ability to give vital hemodynamic measurements in critically ill patients makes their use invaluable when providing quality medical care. The formation of pulmonary artery (PA) pseudoaneurysm from a Swan-Ganz catheter-induced perforation of the PA is a rare but potentially fatal complication of Swan-Ganz catheter use. Three case presentations and a review of the literature are presented.     

Monoclonal antibody to human high-molecular-weight kininogen recognizes its prekallikrein binding site and inhibits its coagulant activity

We developed a mouse monoclonal antibody (MoAb 115-21) to human high- molecular-weight kininogen (HK) that recognizes its prekallikrein binding site (residues 565 through 595 of HK). The corresponding synthesized 31-amino acid peptide (peptide IV) was recently shown to retain native HK's prekallikrein binding property. The same peptide bound factor XI also, although less avidly. Our MoAb recognizes purified HK, peptide IV, and the light chain moiety of HK (where the peptide IV resides), as shown by enzyme-linked immunosorbent assay (ELISA) and Western blotting experiments. The apparent dissociation constant for the HK and MoAb 115-21 interaction was 2.2 nmol/L. It does not recognize low-molecular-weight kininogen (LK) with which HK shares its heavy chain moiety or any antigens in human plasma congenitally deficient in kininogens. The binding of MoAb 115-21 to purified light chain of HK was competitively inhibited by peptide IV. In addition, the antibody inhibits HK-dependent clotting activity of normal human plasma and dextran sulfate-mediated activation of prekallikrein in plasma and retards cleavage of HK in normal plasma after contact activation with dextran sulfate. Also, purified Fab fragments of MoAb 115-21 inhibited the HK-dependent coagulant activity and dextran sulfate-mediated prekallikrein activation in normal plasma. Since the kd for HK-MoAb 115- 21 interaction is ten times lower than that of HK-prekallikrein, our data suggest that binding of MoAb 115-21 to HK's peptide IV site increases the free prekallikrein concentration in plasma and thus results in the decreased efficiency of factor XIIa-mediated activation of prekallikrein. Decreased levels of kallikrein thus formed may be responsible for the inhibition of HK-dependent clotting activity and the decrease in rate and extent of HK cleavage in normal plasma on contact activation with dextran sulfate. MoAb 115-21 may thus prove very useful, especially with its high affinity for HK, in further delineation of the role of HK and prekallikrein in contact activation and kinin-related human pathology.