Metabolic regulation of apoproteins of high-density lipoproteins by estrogen and progesterone in the baboon (Papio sp)

To determine the metabolic regulation of the apoproteins of high-density lipoproteins (HDL) by estrogen and progesterone, 12 ovariectomized and hysterectomized baboons were fed a high cholesterol, high fat diet and were divided into four groups. One of these groups was the untreated control and the remaining three groups were treated with estrogen, progesterone, or a combination of both. After 10 months of treatment, there were significant differences in HDL apolipoprotein (apo) A-I and apo A-II levels in these groups. The apo A-I level was highest in baboons treated with the combination therapy, followed by those treated with estrogen. Baboons treated with progesterone and those in the control group had similar levels of apo A-I. Baboons treated with both estrogen and progesterone and estrogen alone had significantly higher levels of apo A-I than those in the control or progesterone group. Baboons treated with hormones had higher apo A-II levels than controls, and those treated with the combination therapy had the highest level. Metabolic studies suggested that both estrogen and progesterone increased apo A-I and apo A-II production. Progesterone also increased the fractional catabolic rate of apo A-I, but not of apo A-II. On the other hand, estrogen did not affect the fractional catabolic rate of either apo A-I or apo A-II. Thus, increased apo A-I content of HDL in baboons treated with both estrogen and progesterone or estrogen alone appears to be due to increased apo A-I synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transradial right and left heart catheterizations: a comparison to traditional femoral approach.

OBJECTIVES: This study compares the transradial versus transfemoral approach to combined right- and left-heart catheterization. BACKGROUND: Central venous access from peripheral veins has been a historically useful technique. Although the need for right-heart catheterization has been considered an exclusion for transradial catheterization, we have combined a peripheral approach to the central venous system with radial arterial access which permits bilateral heart catheterization using a transradial approach. METHODS: Over an 18-month period all right-heart catheterizations done in conjunction with arterial access were reviewed. Salvage procedures, mixed site access, and biopsy procedures were excluded. Radial procedures were performed using radial artery access and a forearm vein. Femoral procedures used femoral artery/vein. Demographics, procedural information, and postprocedural complications including those requiring vascular ultrasound or transfusion were recorded and used for comparison between groups. RESULTS: Total of 175 femoral/105 radial cases done by 4 operators met criteria for comparison. Both groups had similar procedural indications and age. Procedural durations were shorter (P < .01) with radial 70 +/- 5.0 min (+/-95% CI) vs. femoral 75 +/- 5.4 min (+/-95% CI). Crossover was noted in several patients from both groups; radial procedures (n = 2) failed due to previous shoulder trauma. Femoral crossover to radial involved difficult arterial access. Complications related to access site occurred in 12 femoral and 0 radial patients. CONCLUSIONS: Using the forearm for central venous access appears safer than using the femoral vessels. Transradial catheterizations can be done in combination with forearm venous access procedures with excellent results and enhanced patient safety.     

Alterations during medical interpretation of ICU family conferences that interfere with or enhance communication

RATIONALE: Many conferences in the ICU occur with the families of patients with limited English proficiency, requiring a medical interpreter. Despite the importance of medical interpretation, little is known about the alterations that occur and their effect on communication. OBJECTIVES: This study characterizes the types, prevalence, and potential effects of alterations in interpretation during ICU family conferences involving end-of-life discussions. METHODS: We identified ICU family conferences in two hospitals in which a medical interpreter was used. Ten conferences were audiotaped; 9 physicians led these conferences, and 70 family members participated. Research interpreters different from those attending the conference translated the non-English language portions of the audiotaped conferences. We identified interpretation alterations, grouped them into four types, and categorized their potential effects on communication. RESULTS: For each interpreted exchange between clinicians and family, there was a 55% chance that an alteration would occur. These alterations included additions, omissions, substitutions, and editorializations. Over three quarters of alterations were judged to have potentially clinically significant consequences on the goals of the conference. Of the potentially significant alterations, 93% were likely to have a negative effect on communication; the remainder, a positive effect. The alterations with potentially negative effects included interference with the transfer of information, reduced emotional support, and reduced rapport. Those with potential positive effects included improvements in conveying information and emotional support. CONCLUSIONS: Alterations in medical interpretation seem to occur frequently and often have the potential for negative consequences on the common goals of the family conference. Further studies examining and addressing these alterations may help clinicians and interpreters to improve communication with family members during ICU family conferences.     

Determinants of glucose and ketoacid concentrations in acutely hyperglycemic diabetic patients

Diabetic hyperosmolar coma is a syndrome of marked hyperglycemia and minimal ketoacidosis. In general, the serum glucose concentrations are not predictive of the serum ketoacid concentrations in acutely decompensated diabetes. The endocrine factors that modulate glucose concentrations may be different from those that modulate ketoacid concentrations in patients with acutely decompensated diabetes. To test this hypothesis, regression analysis was used to determine the endocrine and metabolic characteristics that correlated with serum concentrations of glucose and ketoacids in 26 diabetic patients with spontaneous, acute hyperglycemia. All patients had a serum glucose level greater than 390 mg/dl, and ketoacid levels were from 0.17 to 25.5 mM. Multiple regression analysis showed that increased serum glucose concentrations correlated with increased plasma glucagon levels (p = 0.0007, r2 = 0.45), but with no other factors. Increased total ketoacid levels (acetoacetate plus 3-hydroxybutyrate) correlated with increased free fatty acid levels (p = 0.0001), decreased C-peptide levels (p = 0.002), and increased body mass index (p = 0.002) (r2 = 0.72). Body mass index only correlated with ketoacid levels, when it was analyzed with C-peptide and free fatty acid levels. A model is proposed that predicts the serum glucose and ketoacid concentrations in patients with acutely decompensated diabetes. Glucagon modulates the serum glucose concentration in these patients with an absolute or relative insulin deficiency. Total serum ketoacid levels are determined by the serum free fatty acid concentration, residual pancreatic insulin secretion (as reflected by C-peptide), and the patient's body habitus. This model allows for the marked hyperglycemia and minimal ketosis of diabetic nonketotic hyperosmolar coma, as well as the glucose and ketoacid concentrations in other presentations of acutely decompensated diabetes.     

Sera from patients with heparin-induced thrombocytopenia generate platelet-derived microparticles with procoagulant activity: an explanation for the thrombotic complications of heparin-induced thrombocytopenia

Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion. Further studies showed that heparin-induced thrombocytopenia sera also produced a marked increase in procoagulant activity. In contrast, sera from patients with quinine- or quinidine-induced thrombocytopenia did not generate platelet-derived microparticles nor generate increased procoagulant activity. However, quinine/quinidine-induced thrombocytopenia sera produced a significant increase in the binding of IgG to platelets in a drug-dependent fashion, whereas sera from patients with heparin-induced thrombocytopenia demonstrated no drug-dependent binding of IgG to platelets. We also observed increased levels of circulating microparticles in patients with acute heparin-induced thrombocytopenia compared with control patients. Our observations indicate that the generation of procoagulant platelet-derived microparticles in vivo is a plausible explanation for the thrombotic complications observed in some patients with heparin-induced thrombocytopenia.     

End-of-Life Care for Seriously Ill International Patients at a Global Destination Medical Center

Objective

To characterize the end-of-life care of all international patients who died at a global destination medical center from January 1, 2005, through December 31, 2015.

The Lived Experience of Managing HIV and Chronic Pain: Qualitative Interviews with Patients and Healthcare Providers

AIDS and Behavior - People living with HIV (PLWH) experience higher rates of comorbid chronic pain conditions compared to the general population. Managing HIV and chronic pain, two stigmatized...     

Hydrophilic but not hydrophobic bile acids prevent gallbladder muscle dysfunction in acute cholecystitis

The pathogenesis of acute cholecystitis (AC) is controversial. Bile acids may be involved in the pathogenesis of AC because the hydrophobic chenodeoxycholic acid (CDCA) reproduced in vitro the muscle dysfunction observed in AC and was prevented by the hydrophilic ursodeoxycholic acid (UDCA). The present study examined the in vivo effects of UDCA or CDCA on gallbladder muscle dysfunction caused by AC. Guinea pigs were treated with placebo, UDCA, or CDCA for 2 weeks before sham operation or induction of AC by bile duct ligation (BDL) for 3 days. Pretreatment with oral UDCA prevented the defective contraction in response to agonists (acetylcholine [ACh], cholecystokinin 8 [CCK-8], and KCl) that occurs after BDL. Prostaglandin (PG) E(2)-induced contraction remained normal in the placebo and UDCA-treated groups but was impaired in the CDCA-treated group. Treatment with UDCA also prevented the expected increase in the levels of H(2)O(2), lipid peroxidation, and PGE(2) content in the placebo-treated AC group, whereas CDCA caused further increases in these oxidative stress markers. The binding capacity of PGE(2) to its receptors and the activity of catalase were reduced after treatment with CDCA. Treatment with UDCA enriched gallbladder bile acids with its conjugates and reduced the percentage of CDCA conjugates. In contrast, treatment with CDCA significantly decreased the percentage of UDCA in bile. In conclusion, oral treatment with UDCA prevents gallbladder muscle damage caused by BDL, whereas oral treatment with CDCA worsens the defective muscle contractility and the oxidative stress.