Blue toe syndrome: treatment with percutaneous atherectomy

"Blue toe syndrome" refers to digital ischemia of the foot in the presence of palpable or Doppler audible pedal pulses. This clinical syndrome is caused by microembolization to small vessels from a proximal source. The use of percutaneous transluminal atherectomy is described in the treatment of embologenic superficial femoral artery lesions in seven patients. All seven had prompt healing of the ischemic toes, and none required surgical revascularization or amputation. One patient developed a recurrent stenosis at the atherectomy site and had a second episode of digital ischemia, which was treated by means of atherectomy with a larger device. Histologic study of atherectomy specimens suggests that emboli arise from adherent fibrinoplatelet aggregates or thrombus and less often from cholesterol-rich atheromatous plaque. Although either percutaneous transluminal angioplasty or atherectomy can be used to treat the underlying stenosis, percutaneous atherectomy offers the advantage of nonsurgical removal of embologenic material and provides material for histologic study. Percutaneous atherectomy is an effective method of treating embologenic superficial femoral stenoses in patients with ipsilateral blue toe syndrome.     

Distribution of enteric glia and GDNF during gut inflammation

Background  

The enteric glia network may be involved in the pathogenesis of inflammatory bowel disease (IBD). Enteric glia cells (EGCs) are the major source of glial-derived neurotrophic factor (GDNF), which regulates apoptosis of enterocytes. The aim of the study was to determine the distribution of EGCs and GDNF during gut inflammation and to elucidate a possible diminished enteric glia network in IBD.     

Integration of genomics, proteomics, and imaging for cardiac stem cell therapy

Cardiac stem cell therapy is beginning to mature as a valid treatment for heart disease. As more clinical trials utilizing stem cells emerge, it is imperative to establish the mechanisms by which stem cells confer benefit in cardiac diseases. In this paper, we review three methods - molecular cellular imaging, gene expression profiling, and proteomic analysis - that can be integrated to provide further insights into the role of this emerging therapy.     

Dietary administration of an extract from rosemary leaves enhances the liver microsomal metabolism of endogenous estrogens and decreases their uterotropic action in CD-1 mice

We evaluated the effects of a methanol extract from the leaves of the plant Rosmarinus officinalis L. (rosemary) on the metabolism and action of estradiol and estrone. Treatment of female CD-1 mice with 2% rosemary in AIN-76A diet for 3 weeks increased the liver microsomal 2- hydroxylation of estradiol and estrone by approximately 150%, increased their 6-hydroxylation by approximately 30% and inhibited the 16alpha- hydroxylation of estradiol by approximately 50%. Treatment of female CD- 1 mice with 2% rosemary diet for 3 weeks also stimulated the liver microsomal glucuronidation of estradiol and estrone by 54-67% and 37- 56%, respectively. In additional studies, feeding 2% rosemary diet to ovariectomized CD-1 mice for 3 weeks inhibited the uterotropic action of estradiol and estrone by 35-50% compared with animals fed a control diet. The results of this study showed that feeding female mice a 2% rosemary diet increased the liver microsomal oxidation and glucuronidation of estradiol and estrone and inhibited their uterotropic action.      

Increased bile acid pool inhibits cholesterol 7 alpha-hydroxylase in cholesterol-fed rabbits

BACKGROUND & AIMS: Cholesterol feeding unexpectedly inhibits cholesterol 7 alpha-hydroxylase in rabbits. The aim of this study was to explore the mechanism. METHODS: Twenty male New Zealand white rabbits were fed regular chow with and without 2% cholesterol for 10 days followed by 7 days of bile drainage. The activities of hepatic cholesterol 7 alpha-hydroxylase and sterol 27-hydroxylase that control bile acid synthesis in classic and alternative pathways were related to the size and composition of bile acid pool. RESULTS: After feeding cholesterol, plasma and hepatic cholesterol concentrations increased, the bile acid pool doubled (from 254 +/- 44 to 533 +/- 51 mg; P < 0.001), cholesterol 7 alpha-hydroxylase activity decreased 68% (P < 0.01), but sterol 27-hydroxylase activity increased 66% (P < 0.05) with increased cholic acid synthesis (P < 0.01). Bile drainage in the cholesterol-fed rabbits depleted the bile acid pool and stimulated down- regulated cholesterol 7 alpha-hydroxylase activity 11.4-fold (P < 0.001), although hepatic cholesterol remained elevated. Hepatic sterol 27-hydroxylase activity was unaffected. CONCLUSIONS: Feeding cholesterol increased hepatic cholesterol and stimulated sterol 27- hydroxylase and alternative bile acid synthesis, which expanded the bile acid pool and inhibited cholesterol 7 alpha-hydroxylase in rabbits. In distinction, hepatic sterol 27-hydroxylase was insensitive to changes in the bile acid pool. (Gastroenterology 1997 Dec;113(6):1958-65)     

Differential skeletal impact of tenofovir disoproxil fumarate in young versus old HIV-infected adults

Background:

Lower peak bone mass in early adulthood predicts subsequent fragility fractures. Antiretroviral toxicity could contribute to young HIV-infected individuals not achieving adequate peak bone mass.

Objective:

To determine if tenofovir disoproxil fumarate's (TDF) effect on bone mineral density (BMD) differs by age.

Methods:

We examined BMD data at the lumbar spine and hip from AIDS Clinical Trials Group (ACTG) A5224s and ASSERT and randomized treatment-naive studies comparing TDF/emtricitabine versus abacavir/lamivudine (with efavirenz or atazanavir/ritonavir). In this post hoc analysis, we defined the TDF effect as the difference between mean 48-week BMD per cent changes for lumbar spine and hip in individuals randomized to TDF versus abacavir. We used multivariable linear regression to compare the TDF effect in individuals younger and older than 30 years. If TDF effect by age did not differ significantly between studies, we pooled study populations. Otherwise, analyses were conducted separately within each study population.

Results:

Among 652 subjects, 21% were below age 30 years. The relationship between age and TDF effect significantly differed between A5224s and ASSERT (P?=?0.008 for lumbar spine; P?=?0.007 for hip). In A5224s, there was more bone loss with TDF at lumbar spine and hip in subjects under 30 years old versus in older subjects (???4.5% vs ??1.4%; P?=?0.045; ??4.3% vs ??1.6%; P?=?0.026, respectively). There was no significant evidence for this age-associated TDF effect in ASSERT.

Conclusions:

There was heterogeneity in the observed effect of TDF on bone density in young adults compared to older adults, suggesting that further investigation is required to understand the impact of age on BMD decline with TDF.