Publications

OBJECTIVES

Sexually transmitted infection (STI) screening in correctional facilities provides access to people at high risk for STIs who might not be screened elsewhere. These screening programmes are becoming more widespread, but with decreasing funding for STI control, maximising screening impact has become increasingly important. We aimed to make recommendations about the impact of age and sex targeted screening in correctional facilities.

METHODS

We compared the prevalence of chlamydia and gonorrhoea for January 2003-July 2005 among different age groups of females and males screened in San Francisco correctional facilities -- youth detention (12-17 years) and adult jail (18-35 years).

RESULTS

16 975 chlamydia tests and 13,443 gonorrhoea tests were performed. The age specific chlamydia test positivity among females aged 12-17 years, 18-25 years, and 26-30 years, respectively, was 9.6% (105/1092), 9.4% (196/2088), and 6.3% (40/639), compared with 3.3% (100/3065), 6.2% (400/6470), and 3.9% (118/3046) among males. The age specific gonorrhoea test positivity among females in these same age groups was 3.2% (34/1062), 2.7% (57/2082), and 2.4% (15/635), compared with 0.7% (7/1026), 1.2% (67/5507), and 1.0% (25/2555) among males. Of the 1198 STIs identified, 1,020 (85.1%) were treated.

CONCLUSIONS

On the basis of this report and national data, STI control programmes with limited funds should prioritise screening females in youth detention first, women aged < or = 30 years in adult jail second, and men aged < or = 25 years in adult jail third. Males in youth detention should have a lower priority than young adults in jails.

OBJECTIVE

Sphingosine kinase (SphK) is a key enzyme in the synthesis of sphingosine 1-phosphate (S1P), a bioactive sphingolipid. SphK is involved in ischemic preconditioning (IPC). To date no studies in genetically altered animals have examined the role of SphK1 in myocardial ischemia/reperfusion (IR) injury and IPC.

METHODS AND RESULTS

Wild-type and SphK1 null mouse hearts were subjected to IR (50 min global ischemia and 40 min reperfusion) in a Langendorff apparatus. IPC consisted of 2 min of global ischemia and 2 min of reperfusion for two cycles. At baseline, there were no differences in left ventricular developed pressure (LVDP), +/-dP/dtmax, and LV end-diastolic pressure (EDP) between SphK1 mutant and wild-type (WT) mouse hearts. In the mutants, total SphK enzyme activity was reduced by 44% and S1P levels were decreased by 41%. SphK1 null hearts subjected to IR exhibited more cardiac damage compared with WT: LVDP and +/-dP/dtmax decreased, LVEDP increased, and infarct size increased (n=6, P<0.05). Apoptosis was markedly enhanced in SphK1 mutant IR mouse hearts. IPC was cardioprotective in WT hearts, but this protection appeared to be ineffective in SphK1 null hearts. There was no change in infarct size in the IPC+IR group compared to the IR group in the null hearts (50.1+/-5.0% vs 45.0+/-3.8%, n=6, P=NS). IPC remained ineffective in the null hearts even when the index ischemia time was shortened by 10 min.

CONCLUSIONS

Deletion of the SphK1 gene sensitizes the myocardium to IR injury and appears to impair the protective effect of IPC. These data provide the first genetic evidence that the SphK1-S1P pathway is a critical mediator of IPC and cell survival.

RATIONALE

The American Thoracic Society/European Respiratory Society International Consensus Classification panel identified the clinical entity idiopathic nonspecific interstitial pneumonia (NSIP) as a provisional diagnosis and recommended further study.

OBJECTIVES

We hypothesized that idiopathic NSIP is an autoimmune disease and the lung manifestation of undifferentiated connective tissue disease (UCTD), a recently described, distinct entity.

METHODS

We studied 28 consecutive patients with idiopathic interstitial pneumonia (IIP) enrolled in the University of California, San Francisco Interstitial Lung Disease Center who met prespecified criteria for UCTD, as follows: at least one clinical manifestation of connective tissue disease, serologic evidence of systemic inflammation in the absence of clinical infection, and absence of sufficient American College of Rheumatology criteria for another connective tissue disease. Medical record reviews, evaluation of radiographs, and scoring of lung biopsies were performed. The control group consisted of all other patients (n = 47) with IIP who did not meet the UCTD criteria.

MEASUREMENTS AND MAIN RESULTS

The patients with UCTD were more likely to be women, younger, and nonsmokers than the IIP control subjects. Compared with the control group, patients with UCTD-ILD were significantly more likely to have ground-glass opacity on high-resolution computed tomography (HRCT) and NSIP pattern on biopsy, and less likely to have honeycombing on HRCT or usual interstitial pneumonia on biopsy. At our center, the majority of patients classified as idiopathic NSIP (88%) met the criteria for UCTD.

CONCLUSIONS

Most patients diagnosed with idiopathic NSIP meet the case definition of UCTD. Furthermore, these results show that the clinical entity idiopathic NSIP is different from idiopathic pulmonary fibrosis and appears to be an autoimmune disease.