Cytotoxicity of Mycobacterium indicus pranii on Mia-Pa-Ca2 cells

Background: MIP is a cultivable, non-pathogenic organism, which shares several antigens with Mycobacterium tuberculosis and Mycobacterium leprae. It has several proposed clinical applications. However, its cytotoxic effect on pancreatic cancer has not been documented. Hence, the study was conducted to investigate MIP induced cytotoxicity on Mia-Pa-Ca2 cells. To determine the cytotoxic potential of heat killed Mycobacterium indicus pranii (MIP) on pancreatic cancer cells in vitro along with gemcitabine & 5-fluorouracil (5-FU). Mitogen-activated protein kinase (MAPK) level was also studied post MIP treatment. Methods: Cytotoxic effect of MIP, gemcitabine and 5-FU on Mia-Pa-Ca2 cells was determined. We have analyzed extent of apoptosis using flow cytometry and changes in p38 levels, c-Jun N-terminal kinases (JNK) and extracellular signal­regulated kinase (ERK) using ELISA. Results: MIP not only exhibits cell cytotoxicity in dose dependent manner, but also enhances efficacy of gemcitabine and 5-FU when used in combination. Flow cytometry analyses reveals apoptosis of Mia-Pa-Ca2 cells post MIP treatment compared to untreated cells. MAPK pathway study using ELISA shows that p38 and JNK levels are suppressed while there is no change in ERK level. Conclusion: With these results we conclude that MIP is a cytotoxic agent. Cytotoxicity is exhibited by apoptosis. Combining MIP with gemcitabine and 5-FU shows synergistic effect (AU)

Failure of intravenously administered immunoglobulin in the treatment of neonatal myasthenia gravis.

Neonatal myasthenia gravis is uncommon and life threatening. We describe the use of intravenously administered immunoglobulin, in addition to conventional modalities, in a neonate with severe neonatal myasthenia gravis. However, despite this aggressive management, the child had a prolonged period of weakness requiring intensive care.

Anti-pneumococcal antibody levels three to seven years after first booster immunization in children with sickle cell disease, and after a second booster.

We measured pneumococcal antibody levels in 55 patients (ages 7 to 20 years) with sickle cell disease 3 to 7 years after the first booster immunization. Only 6 of the children had protective levels of antibodies (> 300 ng/ml) against all 12 serotypes tested. Thirty-two children (58%) had suboptimal levels against 1 to 3 serotypes; 17 had suboptimal levels against 4 to 10 serotypes. Ten patients from the latter group (ages 13 to 17 years) received a second booster 6 to 8 years after the first booster immunization, and had a marked increase in antibody levels against all serotypes with the exception of serotypes 3 and 4 in two patients and serotype 6A in one patient.

Echocardiography in hypoxemic neonatal pulmonary disease.

Sixteen newborn infants with severe pulmonary parenchymal disease and profound hypoxemia were treated with mechanical ventilation, alkalinization, and intravenous tolazoline. Eight infants responded within two hours of initiation of tolazoline therapy with a rise in Pao2 by at least 100% of pretreatment values (mean = 188%, range = 103 to 427%). Eight infants showed little or no change in Pao2 with administration of tolazoline. Echocardiographic evaluation prior to therapy demonstrated marked elevation in both left (LPEP/LVET = 0.52 +/- 0.13) and right (RPEP/RVET = 0.56 +/- 0.08) ventricular systolic time intervals in the eight infants who subsequently responded to tolazoline. Systolic time intervals in nonresponders were within the normal range (LPEP/LVET = 0.37 +/- 0.03, RPEP/RVET = 0.33 +/- 0.04) and were not significantly different from those observed in a control group of 15 infants with pulmonary disease requiring mechanical ventilation but without hypoxemia. Following tolazoline therapy, systolic time intervals in all eight responders fell to normal values. Echocardiography can provide a safe, noninvasive method for identifying those infants with primary pulmonary disease and severe hypoxemia who could be expected to benefit from tolazoline therapy, thereby avoiding tolazoline side effects in infants for whom tolazoline therapy can be predicted to be of little benefit.

Diagnosis of exocrine pancreatic insufficiency in cystic fibrosis by the synthetic peptide N-benzoyl-L-tyrosyl-p-aminobenzoic acid.

The synthetic peptide N-benzoyl-L-tyrosyl-p-aminobenzoic acid is specifically cleaved by chymotrypsin to Bz-Ty and PABA. The liberated PABA is absorbed and excreted in the urine. Accordingly, PABA recovery reflects intraluminal chymotrypsin activity and is an index of exocrine pancreatic function. This test was evaluated in 24 patients with cystic fibrosis to determine its role in the diagnosis of exocrine pancreatic insufficiency. Cumulative percent PABA recovery in six hours was significantly lower in CF patients compared with the control group. No overlap was noted between the two groups. There was good correlation between PABA recovery, fecal chymotrypsin activity, and coefficient of fat absorption. These findings indicate that PABA recovery is significantly reduced in patients with CF and steatorrhea and may prove a practical and reliable test of pancreatic insufficiency.