Search PubMed⌕ Search

Biomedical subjects

J M Beck

Publications and source records attributed to J M Beck.

At least 37 records · Page 2Linked to original sources
PubMed1997

Small-bowel continuity: a crucial factor in determining survival in gastroschisis.

A retrospective analysis of a series of 63 cases of gastroschisis managed over an 11-year period distinguished a single statistically significant prognostic factor. There were 6 (9.5%) deaths, of which 4 occurred in the 8 infants with small-bowel atresia/stenosis (P < 0.005, Fisher's exact test). One died at 48 h and the remaining 3 of liver disease related to total parenteral nutrition. Of the 4 survivors, 1 developed a late biliary stricture necessitating hepaticoenterostomy but is alive and well aged 4 years. The remaining 3, following initially prolonged hospitalisations and multiple operations, are alive and well after 2, 4 and 7 years. In 3 patients the atresia was not detected at the primary operation. The small number of cases of gastroschisis-associated small-bowel atresia seen in any one unit may conceal the importance of the problem, and limits experience in the approach to management.

Abdominal Muscles↗
PubMed1997

Upregulation of neuropeptides and neuropeptide receptors in a murine model of immune inflammation in lung parenchyma.

The lung is richly supplied with peptidergic nerves that store and secrete substance P (SP), vasoactive intestinal peptide (VIP), and other neuropeptides known to potently modulate leukocyte function in vitro and airway inflammation in vivo. To investigate and characterize neuromodulation of immune responses compartmentalized in lung parenchyma, neuropeptide release and expression of neuropeptide receptors were studied in lungs of antigen-primed C57BL/6 mice after intratracheal challenge with sheep erythrocytes. The concentrations of cytokines in bronchoalveolar lavage (BAL) fluid rose early and peaked on day 1 for interleukin (IL)-2, interferon gamma, and IL-10; days 1 to 2 for IL-6; and day 3 for IL-4, whereas the total number and different types of leukocytes in BAL fluid peaked subsequently on days 4 to 6 after i.t. antigen challenge. Immunoreactive SP and VIP in BAL fluid increased maximally to nanomolar concentrations on days 1 to 3 and 2 to 7, respectively in lungs undergoing immune responses. The high-affinity SP receptor (NK-1 R), and VIP types I (VIPR1) and II (VIPR2) receptors were localized by immunohistochemistry to surface membranes of mononuclear leukocytes and granulocytes in perivascular, peribronchiolar, and alveolar inflammatory infiltrates during immune responses. As quantified by reverse transcription-polymerase chain reaction, significant increases were observed in levels of BAL lymphocyte mRNA encoding NK-1 R (days 2 to 4), VIPR1 (days 2 to 4), and VIPR2 (days 4 to 6), and in alveolar macrophage mRNA encoding NK-1 R (days 2 to 6) and VIPR1 (days 2 to 4), but not VIPR2. Systemic treatment of mice with a selective, nonpeptide NK-1 R antagonist reduced significantly the total numbers of leukocytes, lymphocytes, and granulocytes retrieved by BAL on day 5 of the pulmonary immune response. The results indicate that SP and VIP are secreted locally during pulmonary immune responses, and are recognized by leukocytes infiltrating lung tissue, and thus their interaction may regulate the recruitment and functions of immune cells in lung parenchyma.

Animals↗
PubMed1996

Role of CD8+ lymphocytes in host defense against Pneumocystis carinii in mice.

An improved understanding of host defense against Pneumocystis carinii could provide novel therapeutic modalities directed against this opportunistic pathogen. Immunodeficient mouse models confirm the role of CD4+ lymphocytes in defense against P. carinii, but the role of CD8+ lymphocytes is controversial. BALB/c mice specifically depleted of CD4+ lymphocytes are susceptible to P. carinii, recruiting large numbers of CD8+ lymphocytes to their lungs during infection. Because of this recruitment, we hypothesized that CD8+ lymphocytes could participate in host defense against P. carinii. BALB/c mice were depleted of CD4+ lymphocytes, CD8+ lymphocytes, or both CD4+ and CD8+ lymphocytes. All mice were then inoculated intratracheally with P. carinii. Mice depleted of CD4+ lymphocytes became moderately infected with P. carinii. Mice depleted of CD8+ lymphocytes cleared the inoculum, indicating that CD8+ lymphocytes are unnecessary for defense when CD4+ lymphocytes are available. However, mice depleted of both CD4+ and CD8+ lymphocytes became significantly more intensely infected than mice depleted of CD4+ lymphocytes alone. Therefore, CD8+ lymphocytes participate in defense against P. carinii in vivo during depletion of CD4+ lymphocytes. To determine the mechanisms of this protection, CD8+ lymphocytes were purified from the lungs of CD4-depleted mice during infection. Lung CD8+ lymphocytes proliferated in response to P. carinii antigen and elaborated interferon-gamma in vitro. Thus CD8+ lymphocytes provide defense against P. carinii in vivo, and the elaboration of interferon-gamma likely represents one important mechanism of defense. During states of CD4+ lymphocyte depletion, the modulation of CD8+ lymphocyte function may provide alternative approaches to the host defense against opportunistic pathogens.

Animals↗
PubMed1996

Enteric fistulas and necrotizing enterocolitis.

The incidence, presentation, significance, and outcome of infants with internal enteric fistula formation secondary to necrotizing enterocolitis (NEC) were examined. Of 130 infants with NEC treated during a 7-year period, an enteric fistula developed in five (4%). The gestational age of these patients (3 boys, 2 girls) ranged from 25 to 40 weeks and their birth weight ranged from 800 to 3,460 g. Two had Down's syndrome. Plain abdominal radiographs showed widespread intramural gas in all, and portal vein gas in two. Four patients required early laparotomy, which confirmed extensive intestinal necrosis; a diverting jejunostomy or ileostomy was constructed in three, and the abdomen was closed with drainage in one. Fistulas were diagnosed by contrast radiology between 16 and 51 days after the onset of NEC, and were jejunocolic (2), ileocolic (2), and colocolic (1). They were associated with enteric stricture(s), an inflammatory mass, and clinical signs of intermittent sepsis. One infant with an ileocolic fistula died of sepsis before definitive surgical treatment. Of the four who underwent surgery, two survived after limited intestinal resection, but one of the two with short bowel syndrome died. Enteric fistula formation is a rare complication of NEC. Typically it occurs with colonic stricture(s) and is associated with signs of incomplete bowel obstruction and intermittent sepsis. Resectional surgery is successful, but there appears to be a significant risk of short bowel syndrome.

Birth Weight↗
PubMed1996

Nitric oxide and host defense against Pneumocystis carinii infection in a mouse model.

To investigate whether successful host defense against Pneumocystis carinii is dependent on induction of inducible nitric oxide synthase (iNOS) in alveolar macrophages, immunocompetent mice, mice depleted of CD4 lymphocytes with anti-CD4 antibody, and mice with severe combined immunodeficiency (scid) were inoculated intratracheally with P. carinii. Three weeks later, immunocompetent mice had cleared the organisms completely, while CD4 cell-depleted and scid mice were severely infected (scores, 3.6 +/- 0.2 and 2.8 +/- 0.2, respectively). Inflammation scores were significantly higher in CD4 cell-depleted mice (3.4 +/- 0.2) than in scid mice (0.6 +/- 0.2). Minimal iNOS mRNA was detectable in lung tissue from immunocompetent mice; iNOS mRNA was comparable in scid mice and mice inoculated with PBS but was 6-fold higher in CD4 cell-depleted mice. Immunohistochemistry localized iNOS protein to alveolar macrophages in CD4 cell-depleted mice. Thus, iNOS is an unlikely participant in host defense against P. carinii, because enzyme expression does not correlate with either clearance or severity of infection.

Animals↗
PubMed1996

Pneumocystis carinii pneumonia in scid mice induced by viable organisms propagated in vitro.

Pneumocystis carinii pneumonia remains a major cause of morbidity and mortality in human immunodeficiency virus-infected individuals, despite the widespread use of prophylaxis and the development of new chemotherapeutic agents. The study of P. carinii and of pulmonary host defenses directed against it has been limited by lack of reliable, reproducible methods to obtain pure populations of organisms in useful quantities. While recent success has been achieved with cultures of rat P. carinii organisms, cultures of mouse P. carinii organisms have not been successful. Experiments were performed to determine whether P. carinii organisms derived from mice could be propagated in vitro. Mouse P. carinii organisms, obtained from the lungs of chronically infected athymic mice, were inoculated into spinner flasks containing HEL299 feeder cells seated on microcarrier beads. The numbers of mouse P. carinii organisms increased significantly over 7 days in culture. To test the viability and pathogenicity of these cultured organisms, P. carinii organisms were harvested after 7 days of culture and were inoculated intratracheally into susceptible scid mice. Four weeks after inoculation, scid mice developed uniformly severe P. carinii pneumonia. These studies demonstrate for the first time that mouse P. carinii organisms can be propagated in vitro. Furthermore, cultured mouse P. carinii organisms maintain their pathogenicity in an in vivo model system. This culture system will have important applications in the study of P. carinii biology and in the study of host defenses directed against this important opportunistic pathogen.

Animals↗
PubMed1995

Perinatal death as a consequence of fetal stabbing: was it murder?

At 22 weeks gestation, a fetus received a stab wound to the abdomen when the mother was subjected to a knife attack. Premature labour followed 2.5 weeks later. The baby received full intensive care, but died at 4.5 months of age from complications directly related to the premature birth. The person who committed the assault was indicted with murder of the infant according to the precept of transferred malice. In the absence of any clear legal precedent, the judge ruled that the indictment was not consistent with the principles of criminal law, since the malice directed towards the mother could not be regarded as being transferred to the fetus. This was because the wounding of a non-viable fetus with death following 4 months later did not amount to a deliberate killing, and in addition, it was not the intention of the Defendant at the time of the stabbing to kill the infant.

Journal Article↗
PubMed1995

Impact of chart reminders on smoking cessation practices of pulmonary physicians.

Cigarette smoking remains one of the most preventable causes of premature death in our society, yet only a third to a half of smokers visiting a physician are counseled to quit. In the primary care setting, chart reminders can increase physician smoking cessation counseling rates. It is unclear, however, whether pulmonary physicians require prompting to discuss smoking cessation with patients. We hypothesized that chart reminders would improve the smoking cessation counseling and referral practices in our pulmonary clinic. Chart reviews were performed for two 1-mo periods and documentation of smoking status, counseling, and referrals to smoking cessation clinic were recorded. After the implementation of chart reminders, charts were reviewed at 1, 3, and 8 mo. Chart reminders increased documentation of smoking status from 33 to 83% (p = 0.0001). The proportion of all patients counseled increased from 6.0 to 13.2% (p = 0.01). The improvement in counseling to quit occurred primarily by increasing the identification of active smokers. Pulmonary physicians counseled 70% of smokers to quit once patients were identified as smokers. Chart reminders, an inexpensive and easily implemented smoking cessation intervention, increased the overall number and proportion of patients counseled to stop smoking by increasing the number of identified smokers. This simple intervention can improve counseling in populations at high risk for smoking related lung disease.

Counseling↗
PubMed1994

Accessibility and language characteristics in Catalonia.

The relationship between isolation and language spoken is explored using the example of the spread of Castilian Spanish in the Catalonia region of Spain. "With the help of Geographical Information Systems and characteristics of the road and railway networks, centrality scores for urban municipalities and municipalities near the city of Barcelona have been calculated. The analysis of language characteristics does not show any significant relationship of accessibility on the one hand and the distribution of language characteristics on the other. Instead, Catalonia's linguistic geography is strongly linked with massive in-migration of Castilian-speaking minorities."

Communication↗
PubMed1993

Resolution of pancreatic ascites with octreotide.

A 7 month old infant with pancreatitis and ascites was managed successfully with subcutaneous octreotide and external drainage of a pseudocyst. An endoscopic retrograde cholangiopancreatographic examination showed no congenital abnormality and was consistent with chronic pancreatitis. Octreotide has a possible therapeutic role in pancreatic ascites.

Acute Disease↗
PubMed1993

Alveolar macrophage release of tumor necrosis factor during murine Pneumocystis carinii pneumonia.

Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine produced principally by mononuclear cells, is released in response to a variety of pulmonary pathogens. We hypothesized that release of TNF in the lung is a normal part of the host response to intratracheal challenge with Pneumocystis carinii. To test this hypothesis, we measured TNF in bronchoalveolar lavage fluid (BALF) in normal and CD4-depleted mice at various intervals in acute and chronically infected animals. To assess the cell of origin and the control of TNF release in the lung, we measured mRNA for TNF by a competitive polymerase chain reaction and assessed the capacity of adherence-enriched cells to produce TNF in vitro in response to lipopolysaccharide. Our data demonstrate that TNF peaks at 3 h in both control and CD4-depleted mice after acute challenge with P. carinii and this increase in TNF precedes the influx of inflammatory cells into the lung. TNF levels in BALF return to undetectable levels by day 3. In chronically infected animals, there is a 5-fold increase in mRNA for TNF in adherent cells which is associated with an increased capacity to release TNF in vitro. These data suggest that TNF is a normal host response to P. carinii infection; however, there is no difference in acute TNF release between control animals that clear their infection and CD4-depleted animals that develop chronic infection. TNF is upregulated in chronically infected animals, but CD4 depletion results in the loss of additional host factors essential for resolution of this infection.

Animals↗
PubMed1993

Pulmonary lymphocyte recruitment: depletion of CD8+ T cells does not impair the pulmonary immune response to intratracheal antigen.

CD8+ T cells predominate in the lungs in hypersensitivity and human immunodeficiency virus-related lymphocytic pneumonitis, but their role in the immunopathogenesis of lung disease is unknown. We have shown that in immunized mice depleted of CD4+ T cells, CD8+ T cells are recruited into the lungs in response to intratracheal antigen challenge with sheep red blood cells (SRBC) (J. Clin. Invest. 1991; 88:1244-1254) or to pulmonary infection with Pneumocystis carinii (Am. J. Respir. Cell Mol. Biol. 1991; 5:186-197), suggesting that recruitment of CD8+ T cells does not depend on CD4+ T cell-derived signals. Because CD8+ T cells themselves produce a variety of chemotactic and immunoregulatory cytokines, CD8+ T cells may be important participants in, and modulators of, pulmonary immune responses. To test this hypothesis, we examined the effects of CD8+ T cell depletion on the generation of a pulmonary immune response in vivo. We monitored the recruitment of mononuclear cells into lungs in the absence of CD8-dependent signals and measured the duration of pulmonary inflammation in the absence of suppressor CD8+ T cells. Primed mice were treated with anti-CD8 monoclonal antibody to deplete CD8+ T cells and subsequently were challenged intratracheally with 5 x 10(8) SRBC. At various times after challenge, total and differential cell counts and lymphocyte phenotypes were measured in bronchoalveolar lavage fluid by flow cytometry and lungs were scored histologically. We found that depletion of CD8+ T cells neither decreased recruitment of immune and inflammatory cells nor prolonged the pulmonary immune response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Update: HIV infection and pulmonary host defenses.

Infection with the human immunodeficiency virus (HIV) produces profound alterations in host defense mechanisms throughout the respiratory tract. The extent of alteration of specific defenses varies with the stage or duration of HIV infection in the host. In the upper respiratory tract, HIV-infected individuals have decreased concentrations of salivary immunoglobulin A, which may predispose to colonization of the oropharynx with pathogenic microorganisms. In the lower respiratory tract, host defenses are provided by alveolar macrophages, lymphocytes, and polymorphonuclear leukocytes. Alveolar macrophages can be chronically infected with HIV, and demonstrate a number of compromised host defense functions. The HIV-infected host has a limited capacity to generate soluble signals necessary for activation of alveolar macrophages for microbial killing. CD4 lymphocytes, which are quantitatively depleted during HIV infection, also demonstrate qualitative defects. Proliferation of CD8 lymphocytes, directed against HIV-infected cells in the lung, is associated with the noninfectious pulmonary complications of acquired immunodeficiency syndrome. B lymphocytes from HIV-infected persons show deficient production of opsonizing antibodies, which may predispose to bacterial pneumonias. Defective responses of polymorphonuclear leukocytes in the lung are also likely to contribute to impaired host responses. Collectively, these multiple defects in the defense mechanisms of the respiratory tract explain the unique susceptibility of the HIV-infected host for opportunistic pulmonary infections.

AIDS-Related Opportunistic Infections↗
PubMed1992

Severe anaemia and ileocolic anastomotic ulceration.

Two children are described with anaemia from ileocolic anastomosic ulceration as a late complication of surgery in the newborn period. The anastomosis was revised in each case but in one child there was early recurrence of ulceration.

Anastomosis, Surgical↗
PubMed1991

Reduction in intensity of Pneumocystis carinii pneumonia in mice by aerosol administration of gamma interferon.

Pneumocystis carinii pneumonia in patients with AIDS may result from impaired local release of gamma interferon from lung lymphocytes and subsequent failure of macrophage activation. We tested this hypothesis with mice rendered immunodeficient by selective depletion of CD4+ lymphocytes and inoculated intratracheally with P. carinii. After aerosol administration of recombinant murine gamma interferon, the intensity of P. carinii infection in these mice was reduced in comparison with that in mice not treated with gamma interferon. Histologic scoring of lung tissue did not reveal additional pulmonary inflammation attributable to gamma interferon. Aerosol administration of gamma interferon may reduce the intensity of P. carinii infection by augmentation of host defense, despite persistent CD4+ lymphocyte depletion.

Aerosols↗