Maternal and fetal outcome in preterm premature rupture of membrane

Background: The objective was to study the maternal and fetal outcome in women with premature rupture of membranes.Methods: It was a prospective analytic hospital based study, study population include 100 obstetrics cases of singleton pregnancy with gestational age of 28 week to 36 week with spontaneous rupture of membranes over a period of 2 years, 100 pregnant women without PROM upto 36 completed week taken as control. Detailed clinical examination of the patient was done to see any co-morbidity. Data was collected using a performa. Detailed workup including history, general physical examination, abdominal and pelvic examination and relevant specific investigation were noted.Results: PROM occurs more frequently in primigravida compared to that of multigravida (p=0.679). Risk factors unknown factors 71% and history of coitus 5% UTI (p=0.001) which was highly significant, incidence of LSCS were found higher in PROM than in controls (p<0.05) which was statistically significant. Out of all vaginal deliveries, percentage of patients who had spontaneous labour were 69.86%, while 30.14% were induced, 60% of cases was spontaneous out of which 51% delivered successfully vaginally and, 9% landed in cesarean section. 16% were given prostaglandin gel out of which 10% delivered successfully. 8% were augmented by oxytocin of which 6% delivered successfully and 2% landed in cesarean section. Out of 100 cases studies, 24% accounted for respiratory distress syndrome, while 6% in control group. 12% septicemia in study group (p=0.001) which was highly significant value, while conjunctivitis, neonatal jaundice (hyperbilirubinaemia) and intraventricular haemorrhage accounted for 2%, 3%, and 2% each.Conclusions: Present study concluded that most common cause of PPROM was unknown. Most common maternal morbidity was puerperal fever and neonatal morbidity was respiratory distress. Maternal and fetal morbidity increases with increase in duration between rupture of membranes and delivery of fetus, so augmentation of labour should be done

Role of semen analysis in the diagnosis of infertility at a tertiary care centre in Western India: a prospective study

Background: The prevalence of infertility in the general population is 15%-20%. Of this, the male factor is responsible for 20%-40%. In Indian couples seeking treatment, the male factor is the cause in approximately 23%. Semen analysis is an indispensable diagnostic tool in the evaluation of the male partners of infertile couples. Careful evaluation of the ejaculate parameters may suggest the possible causes of infertility and their identification could help to institute appropriate therapy, if available.Methods: Semen samples were analyzed by manual method. An analysis for volume, viscosity, sperm concentration, motility, and morphology, according to WHO guidelines on semen analysis was done.Results: This study, done at a tertiary care center at Western India, at M.G.M hospital has demonstrated that abnormal semen quality is a major factor contributing to infertility in couples.28% males had volume <2 ml, 70% had sperm count <20 million/ml and 72% had sperms with abnormal morphology.Conclusions: Semen analysis remains a significant contribution in the overall diagnosis of infertility in our environment and semen analysis is an indispensable diagnostic tool in the evaluation of the male partners of infertile couples. Males contribute towards infertility in couples significantly and further study and assessment is required to accurately predict the importance of this

Clinical Correlates of Hepatitis B or Hepatitis C Coinfections in People Living with HIV/AIDS (PLHIV)

Introduction: Hepatitis B virus (HBV) coinfected HIV patients are likely to have chronic hepatitis B infection and associated severe liver disease, however effect of hepatitis B on HIV has not been proven to be off any effect. Similarly in HIV/HCV co-infection majority of the studies have shown no significant influenceof hepatitis C on the course of HIV infection, although some studies have demonstrated an association between HCV infection and faster HIV disease progression.14,15 Therefore, further studies are needed to study the impact of HBV/HCV co-infection on course of HIV, specially, in India.Aims and Objectives: To study the clinical, biochemical and immunological profile of PLHIV co-infected with either hepatitis B or hepatitis C virus, the severity of liver disease and hepatitis B and hepatitis C viral loads in these co-infected PLHIV and the association of WHO stage of HIV and immunosuppression withhepatitis B and hepatitis C viral loads as well as severity of liver disease.Method: It was an observational cross-sectional study, involving 30 PLHIV co-infected with either hepatitis B or C. A detailed history and physical examination was done. Complete Haemogram, Liver function tests, kidney function tests, Ultrasonography abdomen, CD4 cell counts, hepatitis B surface antigen (HBsAg),hepatitis B envelope antigen (HBeAg), hepatitis B Viral DNA (HBV DNA) and HCV RNA levels were done. Severity of liver disease was assessed by FIB 4 SCORE.Results: Among the 30 PLHIV subjects 30% were co-infected with HCV 70% were co-infected with HBV (HBsAg positive). All the subjects were asymptomatic for their liver disease. All the subjects were on Anti-Retroviral Therapy (ART) and 80% were in Early WHO stage (T1 and T2) and 20% were in Advanced WHO stage (T3 and T4). It was similar in both HBV and HCV co-infected group. The mean CD4 count of the subjects was 416.70±189.50 cells/mm3 with the range of 69 – 909 cells/mm3. Five subjects (16.67%) had a CD4 count 3.25). In HCV co-infected subjects 3 of 9 (33.33%) had severe liver fibrosis and only 1 of 21 (4.7%) among HBV co-infected had severe liver fibrosis.Among the 9 HCV co-infected subjects, 3 (33.33%) had undetectable HCV RNA. More number of subjects with detectable hepatitis C viral load had severe liver disease as compared to undetectable viral load.In HIV and HBV co-infected subjects the HBeAg positivity was seen in 42.86% subjects and 38.1% subjects had detectable HBV DNA load. Significant correlation was seen between HBeAg positivity and HBV DNA load. No correlation could be found between FIB 4 score and hepatitis B envelope antigen (HBeAg) positivity or HBV DNA load.No correlation between severity of liver disease (FIB 4) score and WHO staging or CD4 count could be seen. WHO staging and CD4 count also did not correlated with HCV RNA load, HBeAg positivity and HBV DNA load.Conclusions: There is no correlation of CD4 count and WHO stage with liver disease severity or hepatitis viral load in patients on HAART. In HIV and HBV co-infected patients high prevalence of HBeAg positivity is seen. Thus it becomes important to look for deranged liver enzymes and HBeAg positivity in PLHIV coinfected with hepatitis B so that ART can be initiated in these patients irrespective of CD4 count. Hepatitis C co-infected subjects are more likely to have severe liver disease inspite of good CD4 count, so specific treatment for hepatitis C virus should be considered

Immunoprecipitation of spliceosomal RNAs by antisera to galectin-1 and galectin-3

We have shown that galectin-1 and galectin-3 are functionally redundant splicing factors. Now we provide evidence that both galectins are directly associated with spliceosomes by analyzing RNAs and proteins of complexes immunoprecipitated by galectin-specific antisera. Both galectin antisera co-precipitated splicing substrate, splicing intermediates and products in active spliceosomes. Protein factors co-precipitated by the galectin antisera included the Sm core polypeptides of snRNPs, hnRNP C1/C2 and Slu7. Early spliceosomal complexes were also immunoprecipitated by these antisera. When splicing reactions were sequentially immunoprecipitated with galectin antisera, we found that galectin-1 containing spliceosomes did not contain galectin-3 and vice versa, providing an explanation for the functional redundancy of nuclear galectins in splicing. The association of galectins with spliceosomes was (i) not due to a direct interaction of galectins with the splicing substrate and (ii) easily disrupted by ionic conditions that had only a minimal effect on snRNP association. Finally, addition of excess amino terminal domain of galectin-3 inhibited incorporation of galectin-1 into splicing complexes, explaining the dominant-negative effect of the amino domain on splicing activity. We conclude that galectins are directly associated with splicing complexes throughout the splicing pathway in a mutually exclusive manner and they bind a common splicing partner through weak protein–protein interactions

Two forms of ribosomal protein L2 of Escherichia coli that inhibit DnaA in DNA replication

We purified an inhibitor of oriC plasmid replication and determined that it is a truncated form of ribosomal protein L2 evidently lacking 59 amino acid residues from the C-terminal region encoded by rplB. We show that this truncated form of L2 or mature L2 physically interacts with the N-terminal region of DnaA to inhibit initiation from oriC by apparently interfering with DnaA oligomer formation, and the subsequent assembly of the prepriming complex on an oriC plasmid. Both forms of L2 also inhibit the unwinding of oriC by DnaA. These in vitro results raise the possibility that one or both forms of L2 modulate DnaA function in vivo to regulate the frequency of initiation

SR proteins and galectins: what's in a name?

Although members of the serine (S)- and arginine (R)-rich splicing factor family (SR proteins) were initially purified on the basis of their splicing activity in the nucleus, there is recent documentation that they exhibit carbohydrate-binding activity at the cell surface. In contrast, galectins were isolated on the basis of their saccharide-binding activity and cell surface localization. Surprisingly, however, two members (galectin-1 and galectin-3) can be found in association with nuclear ribonucleoprotein complexes including the spliceosome and, using a cell-free assay, have been shown to be required splicing factors. Thus, despite the difference in terms of their original points of interest, it now appears that members of the two protein families share four key properties: (a) nuclear and cytoplasmic distribution; (b) pre-mRNA splicing activity; (c) carbohydrate-binding activity; and (d) cell surface localization in specific cells. These findings provoke stimulating questions regarding the relationship between splicing factors in the nucleus and carbohydrate-binding proteins at the cell surface

Galectin-3C Inhibits Tumor Growth and Increases the Anticancer Activity of Bortezomib in a Murine Model of Human Multiple Myeloma

Galectin-3 is a human lectin involved in many cellular processes including differentiation, apoptosis, angiogenesis, neoplastic transformation, and metastasis. We evaluated galectin-3C, an N-terminally truncated form of galectin-3 that is thought to act as a dominant negative inhibitor, as a potential treatment for multiple myeloma (MM). Galectin-3 was expressed at varying levels by all 9 human MM cell lines tested. In vitro galectin-3C exhibited modest anti-proliferative effects on MM cells and inhibited chemotaxis and invasion of U266 MM cells induced by stromal cell-derived factor (SDF)-1α. Galectin-3C facilitated the anticancer activity of bortezomib, a proteasome inhibitor approved by the FDA for MM treatment. Galectin-3C and bortezomib also synergistically inhibited MM-induced angiogenesis activity in vitro. Delivery of galectin-3C intravenously via an osmotic pump in a subcutaneous U266 cell NOD/SCID mouse model of MM significantly inhibited tumor growth. The average tumor volume of bortezomib-treated animals was 19.6% and of galectin-3C treated animals was 13.5% of the average volume of the untreated controls at day 35. The maximal effect was obtained with the combination of galectin-3C with bortezomib that afforded a reduction of 94% in the mean tumor volume compared to the untreated controls at day 35. In conclusion, this is the first study to show that inhibition of galectin-3 is efficacious in a murine model of human MM. Our results demonstrated that galectin-3C alone was efficacious in a xenograft mouse model of human MM, and that it enhanced the anti-tumor activity of bortezomib in vitro and in vivo. These data provide the rationale for continued testing of galectin-3C towards initiation of clinical trials for treatment of MM