Publications

Previous work has suggested that an extracellular matrix degrading enzyme-matrix metalloproteinase-2 (MMP-2) plays an important role in the development of muscle atrophy. However, the transcriptional regulation mechanism of MMP-2 in skeletal muscle atrophy remains largely unknown. Using transgenic MMP-2 promoter reporter mice, we have demonstrated that AP-1 and RE-1 binding sites in the MMP-2 promoter region, coupled with increased binding of Fra-1, Fra-2 and AP-2, play a critical role in MMP-2 transcriptional regulation in muscle atrophy. Novel information gained from this study has improved our understanding of in vivo transcriptional regulation of MMP-2 in skeletal muscle atrophy.

OBJECTIVES

To determine the contraceptive needs [including emergency contraception (EC)] of women seeking care from a publicly funded sexually transmitted infection (STI) clinic and to better understand women's knowledge of and attitudes towards EC.

METHODS

An anonymous survey was administered to 197 women seeking services at one Chicago Department of Public Health STI clinic.

RESULTS

After excluding women unlikely to become pregnant within the next year because of age, sexual orientation, hysterectomy and those who desired pregnancy (n=47), data from 150 women were available for analysis. Thirteen percent were using "very effective" contraception (intrauterine contraception, implant or sterilization) and 26% were using "effective" contraception (contraceptive pill, patch, ring or injectable). Approximately 23% (95% CI 16.5-30.0%) may have benefited from immediate use of EC as they reported at least one act of unprotected intercourse within the past 5 days.

CONCLUSION

Many women seeking care from public STI clinics are at high risk of unintended pregnancy. A substantial number of women have an immediate need of EC at the time of their clinical visit. Efforts are needed to improve provision of EC as well as effective ongoing contraception for this population.

BACKGROUND & AIMS

Progressive familial intrahepatic cholestasis (PFIC) with normal serum levels of gamma-glutamyltranspeptidase can result from mutations in ATP8B1 (encoding familial intrahepatic cholestasis 1 [FIC1]) or ABCB11 (encoding bile salt export pump [BSEP]). We evaluated clinical and laboratory features of disease in patients diagnosed with PFIC, who carried mutations in ATP8B1 (FIC1 deficiency) or ABCB11 (BSEP deficiency). Our goal was to identify features that distinguish presentation and course of these two disorders, thus facilitating diagnosis and elucidating the differing consequences of ATP8B1 and ABCB11 mutations.

METHODS

A retrospective multi-center study was conducted, using questionnaires and chart review. Available clinical and biochemical data from 145 PFIC patients with mutations in either ATP8B1 (61 "FIC1 patients") or ABCB11 (84 "BSEP patients") were evaluated.

RESULTS

At presentation, serum aminotransferase and bile salt levels were higher in BSEP patients; serum alkaline phosphatase values were higher, and serum albumin values were lower, in FIC1 patients. Elevated white blood cell counts, and giant or multinucleate cells at liver biopsy, were more common in BSEP patients. BSEP patients more often had gallstones and portal hypertension. Diarrhea, pancreatic disease, rickets, pneumonia, abnormal sweat tests, hearing impairment, and poor growth were more common in FIC1 patients. Among BSEP patients, the course of disease was less rapidly progressive in patients bearing the D482G mutation.

CONCLUSIONS

Severe forms of FIC1 and BSEP deficiency differed. BSEP patients manifested more severe hepatobiliary disease, while FIC1 patients showed greater evidence of extrahepatic disease.