Penetrating chest wound: a case report.

An unusual penetrating chest injury was caused by a ball-point pen. Because of apparent penetration of the heart, preparations were made for an emergency open-heart procedure before emergency thoracotomy was undertaken, with the pen still in situ. The pen had bruised the epicardium but had not penetrated the pericardial sac. After removal of the pen, the wound was closed and a chest tube left in place. Recovery, apart from minor degrees of basal atelectasis, pleural effusion and wound infection, was uneventful. The outcome was consistent with that associated with current aggressive management of penetrating chest injuries. Management is based on three approaches. The primary one is intercostal thoracostomy tube drainage and fluid and blood replacement. In cases of massive hemorrhage or air leak, thoracotomy is necessary. The third approach is to prevent post-traumatic pulmonary insufficiency by using fine, high-efficiency filters during blood transfusion, avoiding excessive administration of intravenous fluids, performing tracheostomy after prolonged endotracheal intubation, and using a volume respirator with positive end-expiratory pressure. The average mortality for penetrating wounds of the heart is 25%.     

A detailed serological analysis of a xenogeneic anti-Ia serum

Rabbit anti-mouse-Ia serum was raised against Ia specificities present in CBAJH (H-2 _k) serum. This xenogeneic antiserum was considered to react with similar specificities to those detected by mouse anti-Ia^k alloantisera and more evidence is now presented for this contention. By absorption, the xenogeneic antiserum was found to react with spleen, lymph node, bone marrow, and thymus, reactions similar to that found with the allogeneic anti-Ia^k antiserum. Furthermore, red cells, platelets, brain, kidney, and liver could not absorb the activity from the xenogeneic antiserum, demonstrating the selective tissue distribution of the antigens reactive with this serum. This reactive population was previously shown to consist of B cells and a subpopulation of T cells. In a backcross study of (C57BL/6 × A)F₁ × C57BL/6, the rabbit anti-Ia and mouse anti-Ia reactions were found to segregate together, and some evidence for the genetic regulation of the expression of Ia specificities was also found. By direct testing, and by absorption testing using a number of strains, the xenogeneic antiserum was shown to contain high titers of antibody to Ia.1, 3, 7, 15, and 17; lower titers to Ia.19, and 22; little antibody to Ia.18, and no reaction for the private specificity Ia. 2, although the multiple absorptions required to define these specificities may have observed some reactions. The data indicate that the xenogeneic and allogeneic anti-Ia_k antisera recognize similar Ia determinants, which map to theLA, IE andIC subregions of theH-2 complex. These have been given the same specificity designation as the allogeneic specificities, but they are separately identified by a prime (').     

The extracellular domain of p185/neu is released from the surface of human breast carcinoma cells, SK-BR-3.

The human breast carcinoma cell line SK-BR-3, expresses the neu oncogene product, p185, which is a receptor tyrosine kinase. Using a double monoclonal antibody capture enzyme-linked immunosorbent assay for p185, activity was detected in conditioned media from cultures of SK-BR-3 cells. Two monoclonal antibodies specific for the extracellular domain of p185/neu immunoprecipitated a protein with a molecular mass of approximately 105 kDa. p105 was further shown to compete with p185 for binding to monoclonal antibodies and pulse-chase experiments indicate that it was generated by post-translational processing. Peptide maps showed that p105 and p185 are related polypeptides. Since p105 is close to the predicted size for the extracellular domain of p185/neu, we propose that SK-BR-3 cells specifically process and release this portion of the receptor into the medium. The release of the extracellular domain may have implications in oncogenesis and its detection could prove useful as a cancer diagnostic.     

Lack of glyconeogenesis in pancreatic islets: expression of gluconeogenic enzyme genes in islets.

Studies were performed to obtain evidence for glyconeogenesis from pyruvate to the triose phosphates in pancreatic islets. Inability to show this evidence would be consistent with the fact that glyceraldehyde, but not pyruvate, is a potent insulin secretagogue. Synthesis of 14C-labelled glucose from 14C-labelled pyruvate could not be detected. Since this might have been due to lack of sensitivity required to measure 14C-glucose production in such a scarce tissue as islets, cDNA probes were used to estimate the relative expression of genes coding for gluconeogenic enzymes. Islets expressed pyruvate carboxylase mRNA, but even islets from rats which had been starved (a condition which induces phosphoenolpyruvate carboxykinase (PEPCK) in liver, kidney and adipose tissue) showed no PEPCK mRNA. This is consistent with our previous work showing the absence of PEPCK enzyme activity in islets. Therefore, islets can convert pyruvate to oxalacetate, but since they lack PEPCK, neither the beta nor alpha cell can convert oxalacetate to phosphoenolpyruvate and carry out glyconeogenesis. Pyruvate carboxylase mRNA was increased in islets that possessed the capacity for glucose-induced insulin release versus islets that lacked the capacity to respond to glucose, such as islets from fed rats (versus starved rats) and in islets cultured at a high concentration of glucose (versus at low glucose). Pyruvate carboxylase, therefore, must be involved in pyruvate metabolism and not glyconeogenesis in the pancreatic islet.     

Selection of dieldrin-resistant strains of Lucilia cuprina (Diptera: Calliphoridae) after ethyl methanesulfonate mutagenesis of a susceptible strain.

After ethyl methanesulfonate (EMS) mutagenesis of a susceptible strain (SWT), selective screening of Lucilia cuprina (Wiedemann) resulted in four strains that were resistant to the insecticide dieldrin. Concentrations used for selection were greater than LC99 of susceptible phenotypes. No resistant variants were screened from the standard laboratory strain (SWT) not treated with EMS. The resistance phenotypes of the four resistant strains were similar to each other and to that of a field-selected resistant strain. The genetic basis of resistance is monogenic in all strains and the data are consistent with the same locus, Rdl, determining resistance status in each strain. The Rdl locus maps to chromosome V, approximately 3.5 map units distal to the Sut locus. Dieldrin resistance may be caused by less effective blocking of insect neuronal GABA receptors by the chemical in resistant strains. The data indicate that the evolution of resistance to an insecticide in the field may be constrained by a limited number of genetical and biochemical options if a monogenic response is selected for and that the spontaneous mutation rate to the Rdl allele is less than 1 in 10(6) in the laboratory.     

Production of MUC1 and MUC2 mucins by human tumor cell lines.

A mucus secreting, clonal derivative (HT29-SB) of the human colonic adenocarcinoma cell line HT29, and the LS174T colon cancer cell line, secrete mucin into the culture medium as a viscoelastic gel. Mab BC2, which defines a peptide epitope present in the variable number of tandem repeats (VNTR) of the MUC1 core protein, reacted with this material after deglycosylation. Two high molecular weight bands were detected in TFMSA treated gel-formed mucin from HT29-SB and LS174T by western blotting (Mr 580 kDa and 420 kDa). A similar pattern of reactivity was seen with the culture supernatants from HT29-SB, the ovarian tumor cell line COLO-316, and the breast cancer cell line MCF-7. Mab CCP58 (anti-MUC2 VNTR) reacted with a 580 kDa band in gel-formed mucin produced by LS174T, but was not reactive with mucin produced by the other cell lines. The findings indicate that human colonic cell lines, in addition to breast and ovarian cell lines, may both express and secrete the MUC1 protein core, and that the LS174T cell line expresses and secretes both the MUC1 and MUC2 core proteins.     

Characterization of surface alloantigens of murine neutrophils

Serological analysis of highly purified (>97%) mouse peritoneal exudate neutrophils using a protein-A rosetting technique, showed that these cells possessed the surface phenotype: Ig^–, Thy-1^–, Ly-1^–, Ly-2^–, Ly-3^–, Ly-4⁺, Ly-5⁺, Ly-6⁺, Ly-7^–, Ia^–, FcR⁺ and C3R⁺.     

The human Ia system: Definition and characterization by xenogeneic antisera

The production of xenogeneic anti-Ia serum against Ia antigens in serum has been previously described in the mouse and we now describe the production of xenogeneic anti-human Ia antisera using similar methods. With an indirect resetting technique, Ia-like antibodies were shown to react with the majority of B cells (95%), a subpopulation of T cells, with carbonyl iron adherent cells, and with some E^–Ig^– null cells, but there was no reaction with red cells and platelets. These reactions were the same as those obtained with DRW antisera using cytotoxicity testing. In addition, antigens detected with xenogeneic antisera were also found in serum, where they were found to exist in a low molecular weight, dialyzable form. By the selective removal of different cell surface markers by cocapping, no association could be found with the specifities detected with the xenogeneic anti-Ia antisera and with surface Ig, ₂-microglobulin, or HLA-A and B specificities. Alloantibodies to DRW specificities (but not HLA-A, B specificities) were able to specifically block the binding of the rabbit anti-Ia antibodies to B cells, and reciprocal blocking of rabbit antisera by DRW antibodies was also observed. Several xenogenic antisera were produced by immunizing rabbits with the serum of different individuals. Each antiserum was shown to contain a number of different specificities, as they gave different reaction patterns with different individuals when testing was done both directly and by absorption. These xenogeneic anti-la sera also segregated in a family with HLA-A and B specificities. The detection of a polymorphic antigenic system segregating with the HLA complex, distinct from HLA-A and B specificities, and whose antigens occur predominantly on B cells is therefore described. Because of the similarity of the reactions of the xenogeneic antisera in man to those found in the mouse, and because of the close relationship to the DRW specificities, the system has been provisionally called the H.Ia system.Abbreviations used in this paper AET 2-aminoethyl isothiouronium bromide - ₂-M -2 microglobulin - BSA Bovine serum albumin - H.Ia Human Ia - HuRBC Human red blood cells - Ig Immunoglobulin - Ir Immune response - MHC Major histocompatibility complex - MLR Mixed lymphocyte reaction - NHS Normal human serum - NMS Normal mouse serum - PBL Peripheral blood lymphocytes - PBS Phosphate-buffered saline - RAHIg Rabbit anti-human immunoglobulin - RASIg Rabbit anti-sheep immunoglobulin - RFC Rosette-forming cells - SAHIg Sheep anti-human immunoglobulin - SARIy Sheep anti-rabbit immunoglobulin - SRBC Sheep red blood cells     

Blood-pressure screening and supervision in general practice.

Since April 1975 all men aged 35-69 years registered with four general practices in west central Scotland have had their blood pressure checked whenever they visit the surgery. Although the practice locations range from rural to city centre and observers comprise receptionists, nurses, and doctors, a standard procedure has been adopted for the examination, recording, follow-up, and management of high blood pressure. The results confirm that raised blood pressure is common and often goes undetected. Even when hypertension is known, casual blood pressure readings often exceed accepted normal levels. The findings also show that a population may be routinely examined through normal contact with the family doctor, and that this can provide a convenient, acceptable, and effective means of detecting and reducing raised blood pressure.     

Cooperation between mouse T-cell subpopulations in the cell-mediated response to a natural poxvirus pathogen.

Irradiated CBA anti-DBA/2 cells (10⁶ cells/culture) suppressed the production of effector cells in cultures containing 10⁷ unprimed CBA (responder) and 10⁶ irradiated DBA/2 (stimulator) spleen cells per culture. The suppressive element was cellular and suppression was specific for the stimulating antigen. The suppressive activity resided in the cytotoxic cell population in that both suppressive and cytotoxic activities were found in cells of the same size range, predominantly in T-cells, were produced in response to similar doses of stimulator antigen, and were produced with the same time course following establishment of first sensitization cultures. Eventual suppression correlated with the cytotoxic activity introduced into second sensitization cultures by suppressor cells. The short-term cytotoxic activity and suppressor activity were both highly radioresistant. These studies indicate that the suppressor cells formed in an in vitro mixed lymphocyte culture are cytotoxic to stimulator cells.