Osteoporosis is a condition marked by low bone mineral density and the deterioration of bone tissue. One of the main clinical and economic consequences of osteoporosis is skeletal fractures. To assess the healthcare and work loss costs of US patients with non-vertebral (NV) osteoporotic fractures. Privately insured (aged 18-64 years) and Medicare (aged >/=65 years) patients with osteoporosis (ICD-9-CM code: 733.0x) were identified during 1999-2006 using two claims databases. Patients with an NV fracture (femur, pelvis, lower leg, upper arm, forearm, rib or hip) were matched randomly on age, sex, employment status and geographic region to controls with osteoporosis and no fractures. Patient characteristics and annual healthcare costs were assessed over the year following the index fracture for privately insured (n = 4764) and Medicare (n = 48 742) beneficiaries (Medicare drug costs were estimated using multivariable models). Indirect (i.e. work loss) costs were calculated for a subset of privately insured, employed patients with available disability data (n = 1148). All costs were reported in $US, year 2006 values. In Medicare, mean incremental healthcare costs per NV fracture patient were $US13 387 ($US22 466 vs $US9079; p < 0.05). The most expensive patients had index fractures of the hip, multiple sites and femur (incremental costs of $US25 519, $US20 137 and $US19 403, respectively). Patients with NV non-hip (NVNH) fractures had incremental healthcare costs of $US7868 per patient ($US16 704 vs $US8836; p < 0.05). Aggregate annual incremental healthcare costs of NVNH patients in the Medicare research sample (n = 35 933) were $US282.7 million compared with $US204.1 million for hip fracture patients (n = 7997). Among the privately insured, mean incremental healthcare costs per NV fracture patient were $US5961 ($US11 636 vs $US5675; p < 0.05). The most expensive patients had index fractures of the hip, multiple sites and pelvis (incremental costs of $US13 801, $US9642 and $US8164, respectively). Annual incremental healthcare costs per NVNH patient were $US5381 ($US11 090 vs $US5709; p < 0.05). Aggregate annual incremental healthcare costs of NVNH patients in the privately insured sample (n = 4478) were $US24.1 million compared with $US3.5 million for hip fracture patients (n = 255). Mean incremental work loss costs per NV fracture employee were $US1956 ($US4349 vs $US2393; p < 0.05). Among patients with available disability data, work loss accounted for 29.5% of total costs per NV fracture employee. The cost burden of NV fracture patients to payers is substantial. Although hip fracture patients were more costly per patient in both Medicare and privately insured samples, NVNH fracture patients still had substantial incremental costs. Because NVNH patients accounted for a larger proportion of the fracture population, they were associated with greater aggregate incremental healthcare costs than hip fracture patients.
To test whether the ischemic acute renal failure (IARF) kidney has increased susceptibility to additional ischemic events, IARF was induced in female Sprague-Dawley rats [40 min of bilateral renal artery occlusion (RAO)] and either 18 or 48 hr later, at the height of morphologic injury, they were rechallenged with either 25 or 40 min of RAO. Changes in renal function (GFR, blood flow), morphology, and adenine nucleotide (AN) concentrations in response to these second ischemic challenges were compared to those of normal kidneys subjected to a single ischemic event. In additional experiments, rates of recovery from IARF were compared between rats subjected to one or two bouts of RAO (40 min, 24 hr apart). IARF kidneys retained a significantly greater percent of their baseline GFR and had comparable or higher absolute GFRs after 25 or 40 min of RAO than control rats. IARF rats showed no significant exacerbation of their underlying morphologic injury by superimposing a second ischemic event. IARF kidneys (24 hr post RAO) had normal AN concentrations, and by 30 min of reflow from a second 40 min of RAO, they re-established their AN energy charge and retained AN pools as well as control kidneys. A second 40-min bout of RAO did not significantly prolong recovery rates from the first 40-min ischemic event. In additional experiments, intraperitoneal injection of normal urine or solute matched artificial urine (urea, creatinine, NaCl) into normal rats to mimic the degree of azotemia seen in the IARF rats induced significant and comparable protection against 40 min of RAO. We conclude that the IARF kidney, at or near the height of its functional and morphologic injury, does not have increased susceptibility to additional ischemic insults. Rather a modicum of protection appears to exist, possibly due to renal-failure-induced increments in solute loads per nephron.
Ghee, also known as clarified butter, has been utilized for thousands of years in Ayurveda as a therapeutic agent. In ancient India, ghee was the preferred cooking oil. In the last several decades, ghee has been implicated in the increased prevalence of coronary artery disease (CAD) in Asian Indians due to its content of saturated fatty acids and cholesterol and, in heated ghee, cholesterol oxidation products. Our previous research on Sprague-Dawley outbred rats, which serve as a model for the general population, showed no effect of 5 and 10% ghee-supplemented diets on serum cholesterol and triglycerides. However, in Fischer inbred rats, which serve as a model for genetic predisposition to diseases, results of our previous research showed an increase in serum total cholesterol and triglyceride levels when fed a 10% ghee-supplemented diet. In the present study, we investigated the effect of 10% dietary ghee on microsomal lipid peroxidation, as well as serum lipid levels in Fischer inbred rats to assess the effect of ghee on free radical mediated processes that are implicated in many chronic diseases including cardiovascular disease. Results showed that 10% dietary ghee fed for 4 weeks did not have any significant effect on levels of serum total cholesterol, but did increase triglyceride levels in Fischer inbred rats. Ghee at a level of 10% in the diet did not increase liver microsomal lipid peroxidation or liver microsomal lipid peroxide levels. Animal studies have demonstrated many beneficial effects of ghee, including dose-dependent decreases in serum total cholesterol, low density lipoprotein (LDL), very low density lipoprotein (VLDL), and triglycerides; decreased liver total cholesterol, triglycerides, and cholesterol esters; and a lower level of nonenzymatic-induced lipid peroxidation in liver homogenate. Similar results were seen with heated (oxidized) ghee which contains cholesterol oxidation products. A preliminary clinical study showed that high doses of medicated ghee decreased serum cholesterol, triglycerides, phospholipids, and cholesterol esters in psoriasis patients. A study on a rural population in India revealed a significantly lower prevalence of coronary heart disease in men who consumed higher amounts of ghee. Research on Maharishi Amrit Kalash-4 (MAK-4), an Ayurvedic herbal mixture containing ghee, showed no effect on levels of serum cholesterol, high density lipoprotein (HDL), LDL, or triglycerides in hyperlipidemic patients who ingested MAK-4 for 18 weeks. MAK-4 inhibited the oxidation of LDL in these patients. The data available in the literature do not support a conclusion of harmful effects of the moderate consumption of ghee in the general population. Factors that may be involved in the rise of CAD in Asian Indians include the increased use of vanaspati (vegetable ghee) which contains 40% trans fatty acids, psychosocial stress, insulin resistance, and altered dietary patterns. Research findings in the literature support the beneficial effects of ghee outlined in the ancient Ayurvedic text...
Left-ventricular heart muscle and pectoralis major muscle of the rat were studied to determine the intracellular localization of lactic dehydrogenase (LDH) isoenzymes . Fixation of tissue for 2 hr in 2 % buffered formaldehyde provided the best preservation of the ultrastructure and enzyme activity . Total LDH activity was found diffusely in the ground substance of the sarcoplasm and in the mitochondria of the heart muscle . In skeletal muscle a strong reaction was noted in the sarcoplasmic reticulum, and moderate activity was seen in the ground substance of the sarcoplasm and in the mitochondria . Differentiation of the isoenzymes of LDH was accomplished by addition of 4 M urea or application of heat . Hearttype isoenzymes were mainly localized in the mitochondria and sarcoplasm, whereas muscletype isoenzymes were localized mainly in the sarcoplasmic reticulum of the skeletal muscle . It is speculated that the sarcoplasmic reticulum of the skeletal muscle is the site of anaerobic glycolysis and that the sarcoplasm and mitochondria are involved primarily in aerobic metabolism of pyruvate .
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