Retraction pockets in the tympanic membrane — aetiology and management — our view point

Retraction pockets of the tympanic membrane are believed to be due to eustachian tube obstruction or malfunction. Our observations based on intraoperative findings suggest that the presence of a large sized mastoid antrum along with chronic eustachian tube obstruction plays an important role in the causation of retraction pockets. Granular myringitis may also occur in these circumstances when there is a recurrent eustachian tube blockage due to infection especially if the patient has received frequent and inadequate courses of antibiotics. The use of chromic catgut to create a healed air-filled middle ear space along with a canal wall down tympanomastoidectomy is discussed for their effective treatment.     

Simplified and accurate nonradioactive polynucleotide gene probe assay for identification of enterotoxigenic Escherichia coli.

The present study describes a colony hybridization setup for identification of enterotoxigenic Escherichia coli obviating the need for advanced equipment and radioactive isotopes. With a modest laboratory arrangement, polynucleotide gene probes were produced in large quantities. The probes were labeled with digoxigenin and, after hybridization, detected with an antidigoxigenin alkaline phosphatase conjugate. With an established isotope-based oligonucleotide hybridization assay as reference, a blinded study on a large battery of enterotoxigenic and nonenterotoxigenic bacteria revealed a satisfactory sensitivity and specificity of the nonradioactive assay.     

The Cd40 ligand

For several years, the primary function of CD40 ligand (CD40L) has been believed to be in regulation of contact-dependent, CD40-CD40L-mediated signals between B-and T-cells, which are essential for the regulation of thymus-dependent (TD) humoral immune responses. Recently, a flurry of reports indicate that CD40 is expressed by variety of cell types other than B-cells that include dendritic cells, follicular dendritic cells, monocytes, macrophages, fibroblasts, and endothelial cells. These studies show that CD40-CD40L interactions are important in inflammatory process. For the past few years, through the availability of CD40L-knockout mice, new data have emerged to support the belief that CD40L has many more functions than its role in TD humoral immunity. CD40L-deficient mice have provided significant information towards our understanding of the in vivo role of CD40L. The current picture that emerges indicates that CD40-CD40L interactions mediate many cell-mediated immune responses and T-cell-mediated effector functions that are required for proper functioning of the host defense system. This article focuses on the in vivo role of the CD40L in regulation of cell-mediated effector functions.     

Genetic relationship of putative colonization factor O166 to colonization factor antigen I and coli surface antigen 4 of enterotoxigenic Escherichia coli.

Plasmid DNA from two strains of enterotoxigenic Escherichia coli harboring genes encoding coli surface antigen 4 (CS4) and from seven Indian enterotoxigenic E. coli isolates cross-hybridized at low stringency but not at high stringency with two polynucleotide probes derived from the colonization factor antigen I (CFA/I) operon. Low-stringency Southern blot hybridization of PstI-digested plasmid DNA from the seven Indian isolates yielded characteristic restriction fragment patterns, distinct from those of CS4- and CFA/I-associated plasmid DNA. Two of the Indian strains were transformed with a recombinant plasmid harboring the cfaD gene, which encodes a positive regulator of CFA/I and CS4 genes. The cfaD transformants produced large amounts of putative colonization factor O166 (PCFO166) irrespective of whether the nutrient agar contained bile salts, a growth factor otherwise required for adequate PCFO166 expression. A considerable interstrain variation in the level of PCFO166 production could be explained by differences in the proportion of bacteria that were fimbriated, as visualized by electron microscopy. The N-terminal amino acid sequence of PCFO166 fimbrial protein showed a high degree of homology with the corresponding sequences of CFA/I and CS4.     

Intra-articular morphine versus bupivacaine for postoperative analgesia following knee arthroscopy

In a prospective, double blind, randomized study, 30 ASA I patients were allocated to three groups depending on the drug injected intra-articularly, in an attempt to establish the best postoperative analgesic protocol following knee arthroscopy. Group 1 received 3 mg of preservative-free morphine in 25 ml saline; group 2, 5 mg of preservative-free morphine in 25 ml saline; and group 3, 25 ml 0.25% bupivacaine. The degree of postoperative pain was evaluated by visual analogue scale and the need for additional analgesics at 1, 2, 3, 8 and 24 h. We conclude that bupivacaine 0.25% provides analgesia of early onset and of short duration. While 3 mg-preservative free morphine provides moderate postoperative analgesia with peak effect during the eighth postoperative hour, 5 mg preservative-free morphine provides effective and long lasting (more than 24 h) pain relief. No side effects were noted.     

A contig of non-chimaeric YACs containing the spinal muscular atrophy gene in 5q13

We have constructed a contig of non-chimaeric yeast artificialchromosomes (YACs) across the candidate region for childhoodautosomal recessive spinal muscular atrophy (SMA) In 5q13. Anovel microsatellite reduces the candidate region to approximately400kb of DNA distal to D5S435. The candidate region containsblocks of chromosome 5 specific repeats which have copies on5p as well as elsewhere on 5q. Restriction mapping of the YACsreveals at least one CpG island In the SMA gene region. TheYAC maps indicate that the contig contains minimal rearrangementsor deletions. The data show the value of screening several YAClibraries simultaneously in order to construct a set of overlappingsequences suitable for candidate gene searches and direct genomicsequencing.     

Hindrance of binding to class II major histocompatibility complex molecules by a single amino acid residue contiguous to a determinant leads to crypticity of the determinant as well as lack of response to the protein antigen.

The immune system has evolved the potential to respond to a wide variety of antigens, yet unresponsiveness to many foreign determinants is encountered frequently. Here, we report a lack of response to a particular determinant, hen egg lysozyme (HEL)-(46-61)-peptide (p46-61), in C57BL/6 (H-2b) mice, whereas a strong T-cell response to this determinant is obtained in major histocompatibility complex (MHC)-identical C3H.SW mice. However, (C3H.SW x C57BL/6)F1 mice respond well to p46-61, suggesting the absence of a p46-61-specific "hole" in the T-cell repertoire in C57BL/6 mice. We further show that p46-61 cannot bind the I-Ab class II MHC molecule, whereas p46-60 lacking Arg61 exhibits good binding and is immunogenic in both strains. Thus, the presence of the hindering residue, Arg61, renders p46-61, a dominant determinant in C3H.SW, into a silent, cryptic determinant in C57BL/6 mice. Upon i.p. immunization with HEL, no T-cell responses to either HEL or p46-61 could be demonstrated in spleens of HEL-primed C57BL/6 mice, whereas a predominant response to p46-61 and HEL was demonstrated in C3H.SW mice. Evidently, C57BL/6 mice differ from C3H.SW in their ability to process p46-61 into an actual I-Ab binding determinant, indicating a putative enzymatic defect in the C57BL/6 strain. Furthermore, our results suggest that the inability of C57BL/6 mice to respond in the spleen to HEL is based upon its failure to generate a dominant immunogenic determinant from HEL, coupled with its pattern of susceptibility to regulatory effects.