APACHE II and ISS scores as predictors of nosocomial infections in trauma patients

BACKGROUND: Nosocomial infections affect more than 2 million patients annually in the United States at a cost of $4.5 billion. The aim of this study is to identify the role of the APACHE II score and the Injury Severity Scale (ISS) as independent predictors of nosocomial infections in trauma patients admitted to the intensive care unit (ICU). METHODS: A retrospective chart review of 113 trauma patients admitted to the ICU was conducted by an infectious disease physician. Demographic data and incidence of nosocomial infections were recorded. Multivariate logistic regression analysis was used to determine variables that are predictive of the occurrence of nosocomial infections. RESULTS: Presence or absence of intubation, ICU length of stay, APACHE II score, and ISS were related to the presence of infections; however, only the ICU length of stay was an independent predictor of a nosocomial infection, with an odds ratio of 1.81. By linear regression, 17% of the variance in the ICU duration of stay was a result of the APACHE II score in patients with a score >/=5. CONCLUSION: APACHE II score and ISS score were not good predictors of the incidence of nosocomial infections in trauma patients admitted to the ICU, but the APACHE II score has a modest correlation with the duration of stay in the ICU. A stratified cohort study could identify the subset of patients for which the APACHE II score predicts a prolonged stay in the ICU, thus an increased risk of infection.     

Molecular genetic alterations in carcinoma ex-pleomorphic adenoma: a putative progression model?

To determine the genetic changes associated with the development of carcinoma ex-pleomorphic adenoma (Ca Ex-PA), we analyzed 15 microsatellite loci at chromosome arms 8q, 12q, and 17p on DNA from 26 neoplasms (including 8 microdissected benign and malignant components), and 13 pleomorphic adenomas for comparison. Pleomorphic adenomas and the adenoma component of Ca Ex-PAs showed a higher incidence of loss of heterozygosity (LOH) at chromosome arms 8q (52%) and 12q (28%) than at 17p (14%) loci. In the carcinoma component, the combined LOH at chromosome arm 8q, 12q, and 17p regions was 69%, 50%, and 69%, respectively; within these chromosomal regions, 8q11.23-q12 (42%), 12q23-qter (39%), 17p13 (41%), and 17p11 (45%) loci manifested the highest incidence of LOH. Eight carcinomas (30.7%) showed loss at all three chromosomal arms tested. Of the eight microdissected Ca Ex-PAs analyzed, four adenoma and corresponding carcinoma components (50%) had the same LOH at 12q loci and additional LOH at 17p loci only in carcinomas. Chromosome arm 17p alterations correlated significantly with high disease stage and an increased proliferative rate in these tumors. Our results indicate that alterations at regions on chromosome arms 8q and/or 12q may constitute early events associated with pleomorphic adenomas; that LOH at 12q loci may identify a subset of adenoma with potential progression to carcinoma; that acquisition of additional alterations at chromosome arm 17p loci might represent an event preceding malignant transformation and progression; and that 8q, 12q, and 17p regions may harbor tumor suppressor genes involved in the genesis of PA and Ca Ex-PA. Genes Chromosomes Cancer 27:162-168, 2000.     

Generation of attenuated Mycobacterium bovis strains by signature-tagged mutagenesis for discovery of novel vaccine candidates

Mycobacterium bovis, a member of the Mycobacterium tuberculosis complex, has a particularly wide host range and causes tuberculosis in most mammals, including humans. A signature tag mutagenesis approach, which employed illegitimate recombination and infection of guinea pigs, was applied to M. bovis to discover genes important for virulence and to find potential vaccine candidates. Fifteen attenuated mutants were identified, four of which produced no lesions when inoculated separately into guinea pigs. One of these four mutants had nine deleted genes including mmpL4 and sigK and, in guinea pigs with aerosol challenge, provided protection against tuberculosis at least equal to that of M. bovis BCG. Seven mutants had mutations near the esxA (esat-6) locus, and immunoblot analysis of these confirmed the essential role of other genes at this locus in the secretion of EsxA (ESAT-6) and EsxB (CFP10). Mutations in the eight other attenuated mutants were widely spread through the chromosome and included pks1, which is naturally inactivated in clinical strains of M. tuberculosis. Many genes identified were different from those found by signature tag mutagenesis of M. tuberculosis by use of a mouse infection model and illustrate how the use of different approaches enables identification of a wider range of attenuating mutants.     

Neural Control of Non-vasomotor Organs in Hypertension

Hypertension affects over 25 % of the population with the incidence continuing to rise, due in part to the growing obesity epidemic. Chronic elevations in sympathetic nerve activity (SNA) are a hallmark of the disease and contribute to elevations in blood pressure through influences on the vasculature, kidney, and heart (i.e., neurogenic hypertension). In this regard, a number of central nervous system mechanisms and neural pathways have emerged as crucial in chronically elevating SNA. However, it is important to consider that “sympathetic signatures” are present, with differential increases in SNA to regional organs that are dependent upon the disease progression. Here, we discuss recent findings on the central nervous system mechanisms and autonomic regulatory networks involved in neurogenic hypertension, in both non-obesity- and obesity-associated hypertension, with an emphasis on angiotensin-II, salt, oxidative and endoplasmic reticulum stress, inflammation, and the adipokine leptin.     

Cerebral vasoreactivity: impact of heat stress and lower body negative pressure

Objective

Cerebrovascular reactivity represents the capacity of the cerebral circulation to raise blood flow in the face of increased demand, and may be reduced in some clinical and physiological conditions. We tested the hypothesis that the hypercapnia-induced increase in cerebral perfusion is attenuated during heat stress (HS) compared to normothermia (NT), and this response is further reduced during the combined challenges of HS and lower body negative pressure (LBNP).

Methods

Ten healthy individuals (9 men) undertook rebreathing-induced hypercapnia during NT, HS, and HS + 20 mmHg LBNP (HS_LBNP), while cerebral perfusion was indexed from middle cerebral artery blood velocity (MCA V _mean). Cerebrovascular responses were calculated from the slope of the change in MCA V _mean and cerebral vascular conductance (CVCi) relative to the increase in end tidal carbon dioxide ( \( {\text{PET}}_{{{\text{CO}}_{ 2} }} \) ) during rebreathing.

Results

MCA V _mean was similar in HS (55 ± 19 cm s^?1) and HS_LBNP (52 ± 16 cm s^?1), and both values were reduced relative to NT (66 ± 20 cm s^?1), yet the rise in MCA V _mean per Torr increase in \( {\text{PET}}_{{{\text{CO}}_{ 2} }} \) during rebreathing was similar in each condition (NT: 2.5 ± 0.6 cm s^?1 Torr^?1; HS: 2.4 ± 0.8 cm s^?1 Torr^?1; HS_LBNP: 2.1 ± 1.1 cm s^?1 Torr^?1). Likewise, the rate of increase in CVCi was not different between conditions (NT: 2.1 ± 0.65 cm s^?1 mmHg^?1100 Torr^?1; HS: 2.4 ± 0.8 cm s^?1 mmHg^?1 100 Torr^?1; HS_LBNP: 2.0 ± 1.0 cm s^?1 mmHg^?1 100 Torr^?1).

Interpretations

These data indicate that cerebrovascular reactivity is not compromised during whole-body heat stress alone or when combined with mild orthostatic stress relative to normothermic conditions.