Are the floral morphology and anatomy of Galphimia australis, an atypical neotropical Malpighiaceae, associated to a new pollination syndrome?

The flowers of the species of Malpighiaceae in the Neotropical Region are relatively uniform in their morphology due to their dependence on oil-collecting bees as their main pollinators. However, many species of the genus Galphimia seem to have acquired a different floral syndrome, lacking markedly zygomorphic flowers and developed elaiophores in the calyx. Likewise, these species present anthers with great development, probably in response to the selection of pollinators that collect pollen. Galphimia australis incorporated some of these traits but also retained some residual characteristics typical of species pollinated by oil bees. This leads to many questions on how these flowers ensure their pollination. Inquiring about the reduction or modification of these characteristics allows us to understand how G. australis achieves a different pollination syndrome. In this research, we carry out a detailed morphological and anatomical study of the flowers and pollen grain devolvement of G. australis and floral visitors were observed and captured. Results were analyzed in order to determine how this species changed from the oil-floral syndrome, typical of neotropical Malpighiaceae, to one syndrome with pollen as the main reward.

Comparative push-out test of dense HA implants and HA-coated implants: findings in a canine study.

Two types of hydroxyapatite (HA) implants have been developed: an HA-coated implant and a dense HA implant. For a longer in situ life span, the HA implant must remain chemically stable and possess high resistance to occlusal force. To determine which type of HA implant shows better durability, this comparative dog study was done to evaluate push-out test results of HA-coated implants and dense HA implants of approximately the same size after implantation in the mandibular and coxal bones for periods ranging from 3 weeks to 10 months. The findings revealed that for the mandibular implants, the push-out values of HA-coated implants were significantly higher than those of dense HA implants at 2 and 4 months after implantation, with significance levels of p < .001 and p < 0.05, respectively. However, there was no significant difference between the two implant types at 10 months. As for the coxal implants, no significant differences were noted for any period. Furthermore, the ratio of push-out values of the dense HA implants to those of the HA-coated implants situated in the same position bilaterally in each bone of the body for each implantation period rose with the passage of time, especially in the mandible. In the mandibular implants, the correlation coefficient of the relationship between the ratio and duration of implantation was highly significant (p < 0.001). Push-out testing caused detachment of the surface portion of the HA coating that was bound to the dense bone from the HA-coated implant at 2, 4, and 10 months after implantation. Furthermore, at 10 months the HA-coated layer in the wide areas of the implants had completely detached from the metal substrate, in contrast to the dense HA implants, which remained durable throughout the test period.

Dyslipidemia and coronary artery disease.

Genetically determined and metabolically induced disturbances in lipid metabolism, as manifested in several types of dyslipidemia, have been shown to be causally related to the development of coronary artery disease (CAD). A diversity of clinical and angiographic studies has been made to evaluate the linkage between plasma lipid-control therapy in the development of initial and recurrent cardiovascular events. The plan of treatment invariably begins with a low-fat, low-cholesterol diet before initiation of drug therapy. However, many patients have difficulty in adhering to the low-fat diet. Fortunately, metabolic studies show that foods which contain fats rich in stearic (saturated) and oleic (monounsaturated) fatty acids may be given in limited amounts to boost patients' compliance to a low-fat diet and to prevent their blood lipids from rising to abnormal levels. A bile acid sequestrant (cholestyramine or colestipol) is the first-line drug for control of hypercholesterolemia. Either gemfibrozil or gemfibrozil plus niacin is prescribed to raise high-density lipoprotein (HDL) levels of CAD patients. Approval of two HMG CoA reductase inhibitors, pravastatin and simvastatin, by the FDA gives physicians the additional flexibility of employing a single or a combination drug therapy for optimal control of dyslipidemia. The association of low serum cholesterol level (< 160 mg/dl) with increase in noncardiac mortality has prompted health professionals to consider modifying the universal screening and treatment of serum cholesterol in children and young women and to use hypolipidemic drugs in patients judiciously.

A histologic comparison of the functional loading capacity of an occluded dense apatite implant and the natural dentition.

A histologic comparison of the functional loading capacity of an occluded dense apatite implant and the natural dentition at a ratio of one implant to three natural teeth was carried out on six monkeys. Single implants were placed in the maxillary left second molar and mandibular right second molar of each monkey. Four months later, the vertical dimension of occlusion was raised at the contacting areas between the implant and the connected first, second, and third opposing molar teeth by placing metal crowns on them. The three connected molars gradually intruded over time, whereas the supporting bone of the mandibular and maxillary implants showed no abnormalities and was able to bear the load because of thickening and remodeling of the surrounding bone.

[Histological study on occlusal bearing capability of apatite implant in maxilla].

The focus of this study is aimed on the degree of occlusal bearing capability of the dense apatite implant in the maxilla and its histological alteration. The implants were placed in the [symbol: see text] areas of the adult monkeys. The vertical dimension was raised by the implants, the opposite [symbol: see text] were splinted together with the connected crowns. At 1, 3 and 7 months after loading, the tissue surrounding the implants and opposing [symbol: see text] was examined histologically with the following results: 1. The formed and newly compacted lamellae and woven bone were seen along the implant supporting the trabeculae and the compact bone that supports the implant and gradually getting thicker until the third month. 2. Realignment and remodelling of the trabeculae and compact bone continuously progressed from 3 months onward. 3. Bone formation and bone remodelling were also observed to have progressed widely towards the neighboring teeth, and bone remodelling in the maxillary sutures similarly occurred. 4. The splinted opposite teeth intruded gradually during the experiment. 5. In some implants, few fracture areas close to the surface were observed in the bone that was in contact with the implant.

Efficacy and safety of pravastatin in patients with primary hypercholesterolemia. II. Once-daily versus twice-daily dosing.

This 8-week multicenter, placebo-controlled trial compared the efficacy and safety of the HMG-CoA reductase inhibitor, pravastatin, when administered either as single doses of 40 mg in the morning (AM) or evening (PM) or 20 mg twice daily (bid) in 196 diet-stabilized outpatients with primary type II hypercholesterolemia. Mean reductions in total and low-density lipoprotein (LDL) cholesterol concentrations were observed in all pravastatin groups after 1 week and were sustained throughout the study (P less than or equal to 0.001 versus baseline and placebo). At week 8, mean reductions from baseline in the pravastatin treatment groups were 23-27% for total cholesterol and 30-34% for LDL cholesterol. LDL cholesterol was reduced greater than or equal to 15% by pravastatin in all patients in the group treated with 40 mg PM and in 88 and 96% in those receiving 20 mg bid and 40 mg AM, respectively. High density lipoprotein cholesterol was elevated (up to 8%) and triglycerides were reduced (up to 25%) by all pravastatin regimens (P less than or equal to 0.05). Pravastatin was well tolerated and was associated with a low incidence of adverse events. No patient withdrew from the study due to a pravastatin-related adverse event. Once-daily pravastatin is a safe and effective treatment for patients with primary hypercholesterolemia and has a favorable safety profile.

Serum lipids after gastric bypass surgery for morbid obesity.

Thirty-eight of 151 consecutive patients (25 percent) undergoing bypass surgery for morbid obesity had increased serum levels of total cholesterol (TC), triglycerides (TG) or both preoperatively. Ten patients had isolated TC elevation, six had isolated TG elevation and 22 had both TC and TG elevation. High density lipoprotein-cholesterol (HDL-C) levels were subnormal in 28 of the 38 patients (74 percent). Fasting lipid profiles were determined in the 38 hyperlipidemic patients at 6-month intervals postoperatively. Mean follow-up period was 29 months. By 6 months postop, patients had a greater than or equal to 20 percent mean reduction in TC and greater than or equal to 50 percent mean reduction in TG which were significant in comparison with preop levels and correlated with weight loss (P less than or equal to 0.05). Mean HDL-C levels had increased significantly vs. preop levels by 12 months postop (P less than 0.05). Lipid profiles became normal in 32 of the 38 patients (84 percent). Improvements in lipid profile were sustained in all patients with satisfactory weight loss but regressed after 12 months in patients who did not lose greater than or equal to 50 percent of their excess weight. These results suggest that abnormal serum lipid profiles can be permanently improved with sustained weight loss after gastric restriction surgery for morbid obesity.

Suppression of aortic atherosclerosis in cholesterol-fed rabbits by purified rabbit interferon.

The effectiveness of rabbit interferon in suppressing atherosclerosis was evaluated in rabbits fed a diet containing 1% cholesterol. Ten male New Zealand White rabbits received intramuscular injections of 1 million units of interferon twice a week, while a control group of 10 rabbits received injections of buffer. Both groups had average serum cholesterol levels of over 2000 mg/dl during the 8-week experimental period. Interferon treatment resulted in no significant hypolipidemic effect or changes in lipoprotein composition. Atherosclerotic lesions in aortas were quantified both macroscopically and microscopically. Interferon treatment decreased the grossly visible lesion area significantly from 25 +/- 4% to 8 +/- 1% (mean +/- SEM, p less than 0.005) compared to the untreated group. Microscopic analysis of serial cross-sections of aortic segments revealed significant (p less than 0.01) reductions in both lesion size and frequency in the interferon-treated group. Electron microscopy also showed that interferon treatment reduced the pathological effects of cholesterol feeding. Tissue analysis showed that total aortic cholesterol was reduced by 28% by interferon treatment, while the aortic phospholipid concentration was increased by 25%. The possibility exists that the interferon preparation used contained other biological response modifiers and that the observed effects may be totally unrelated with interferon. These results suggest that the mechanism of atherosclerosis suppression in these cholesterol-fed rabbits is not related to the lowering of serum cholesterol but may be associated with inhibition of lesion initiation.

Management of blood lipid abnormalities in coronary heart disease patients.

Information obtained from clinical and laboratory research strongly supports a causal relationship between hyperlipidemia (dyslipidemia) and coronary heart disease (CHD), and provides an impetus to develop strategy for control of dyslipidemia. Some recent developments in the field may include the use of: (1) colestipol-niacin to control hypercholesterolemia and induce regression of coronary atherosclerosis; (2) limited amounts of foods rich in stearic or oleic fatty acids to enhance the appeal of cholesterol-lowering regimen; (3) gemfibrozil or lovastatin to inhibit cholesterol synthetic activity; and (4) gemfibrozil to raise atherosclerosis-protective plasma high-density lipoprotein levels. These and other newer developments will stimulate interest in research on dyslipidemia and its control to facilitate primary and secondary prevention of CHD.

Treatment of type III hyperlipoproteinemia with gemfibrozil to retard progression of coronary artery disease.

Eight type III hyperlipoproteinemic (type III HLP), homozygous E 2/2 patients were enrolled in two periods of long-term diet-gemfibrozil treatment. The combined therapy resulted in highly significant decreases in their low-density lipoprotein cholesterol, very-low density lipoprotein cholesterol, very-low density lipoprotein triglycerides, and increases in their high-density lipoprotein cholesterol during the first treatment period of 24 to 28 months. Type III HLP reasserted itself following an 8-week interruption of gemfibrozil therapy. Resumption of gemfibrozil therapy again lowered the high lipid-lipoprotein concentrations of these patients toward normal. Tuboeruptive xanthomata, palmar xanthoma, and xanthoma striata palmare subsided with treatment. Follow-up coronary arteriograms performed 2.5 to 3.0 years after initiation of diet-drug treatment showed stabilization of coronary arterial lesions, which was associated with improvement in exercise tolerance.

Extracranial carotid arterial disease in patients with familial hypercholesterolemia and coronary artery disease treated with colestipol and nicotinic acid.

Carotid bifurcation atherosclerosis was demonstrated in 34 of 108 patients with familial hypercholesterolemia and coronary artery disease by B-scan, continuous-wave Doppler sonography, and intravenous digital subtraction angiography. An intensive combined therapy of diet, colestipol, and nicotinic acid was mounted to control the hypercholesterolemia of these patients. Their serial sonographies and digital subtraction angiography were evaluated independently by technical specialists who served as coinvestigators. The data obtained suggest that extracranial arterial disease can develop concurrently with coronary artery disease in a significant proportion of patients with familial hypercholesterolemia, and amaurosis fugax, transient ischemic attack, cerebral infarction, and myocardial infarction did not recur during 58-72 months of control of familial hypercholesterolemia in this series of patients.

Monoclonal antibodies against antigens expressed on human hepatocellular carcinoma cells.

Monoclonal antibodies with selectivity for human hepatoma cell lines were produced by immunizing BALB/c mice with human hepatoma cell lines, HA22T/VGH or Hep 3B, and fusing sensitized mouse spleen cells with mouse myeloma cells. Two monoclonal antibodies recognizing antigens present only on human hepatoma cell lines were investigated. The monoclonal antibody IB1 was found to react with 3 of 9 hepatoma cell lines. Monoclonal antibody 9B2 reacted with all nine hepatoma cell lines. None of the other 20 cell lines tested was bound by IB1 and 9B2. The immunoperoxidase staining of monoclonal antibodies on frozen sections of paired hepatoma and normal liver tissues from the same individuals were studied. Antibody IB1 reacted with 3 of 13 hepatoma tissues, but with none of the normal liver and other tissues, and antibody 9B2 was reactive with antigens appearing on the bile canalicular domain of hepatoma and normal liver tissues. The antibody 9B2 stained no normal tissues with the exception of proximal tubules of kidney. Radioimmunoprecipitation tests identified two antigens reacting with 9B2. The major antigen had an apparent molecular weight of 140,000 and a minor one of 130,000. Therefore, antibody IB1 seems to be specific for antigens present on a group of human hepatoma cells and may be useful for classification and diagnosis of human hepatomas. Antibody 9B2 is quite specific to human liver cells and may be used to provide clues for the characterization of tumor cell lines, identification of metastatic tumors with hepatocytic origin, and study of the structure and function of bile canaliculi.

Effects of combined probucol-colestipol treatment for familial hypercholesterolemia and coronary artery disease.

To evaluate the effect of hypercholesterolemic treatment on coronary artery disease in patients known to be susceptible to disease progression, 44 patients with familial hypercholesterolemia and coronary artery disease were started on a lipid-lowering diet and either probucol (1 g/day) or colestipol (30 g/day). After 5 months of monotherapy, all patients went on a regimen of diet and 2-drug therapy. To date, combination therapy has continued for 3.4 to 4.1 years, and has resulted in the following changes from baseline in mean serum lipid levels: -48.5% in total cholesterol, -53.3% in low density lipoprotein cholesterol, -30.0% in high density lipoprotein cholesterol and +14.5% in triglycerides. The reduction in low density lipoprotein cholesterol apparently improved the clinical status of these patients despite the associated drop in high density lipoprotein cholesterol. In the 19 patients who underwent coronary arteriography before admission to the study, follow-up arteriograms showed that combined treatment stabilized the progression of established lesions and prevented the formation of new ones. Side effects occurred mainly with monotherapy and during the early phase of combination therapy. Reactions included diarrhea, constipation, other vague abdominal symptoms, headache and joint stiffness. In all instances, the side effects gradually subsided after the institution of combination therapy. The combination of probucol and colestipol plus diet appears to be effective in treating most patients with familial hypercholesterolemia.

When and how to treat hyperlipidemia.

The recently completed NHLBI sponsored multicenter double-blind Coronary Heart Disease Prevention Trial has provided the long sought-after proof that hyperlipidemia is a major CAD risk factor and that the incidence of CHD and its complications can be favorable modified by control of hyperlipidemia with appropriate diet-drug therapy. This nationwide study confirms and validates the earlier reports on the feasibility to stabilize or to promote regression of atherosclerotic arterial lesions through hyperlipidemia control. Current investigations suggest that in most instances, simple differentiation of hyperlipidemias into hypercholesterolemia and hypertriglyceridemia (major components of low-density and very low-density lipoprotein) can supply adequate information for clinical practice. In difficult-to-control hyperlipidemias, the application of lipoprotein analysis may provide insight of the underlying genetic-metabolic abnormality for selection of more specific therapeutic modality. Before considering hypolipemic therapy, secondary hyperlipidemias should be excluded. In those cases, treatment should be directed to the primary disease(s) for the solution of the hyperlipemic problem. Life-long dietary modification is the key step to treatment of all types of hyperlipidemias, and especially the primary hyperlipidemias. In this latter group, both the patient and the family should be educated on the principles and the importance of dietary modification to boost compliance. In familial hyperlipidemias, a specifically effective hypolipemic drug, or a combination of drugs with minimal or no long-term toxic and side effects, should be prescribed to augment the therapeutic diet to lower the elevated plasma lipid levels and stabilize them at normal range. Early detection and control of atherosclerosis-prone hyperlipidemias in children and young adults should be vigorously promoted to improve cardiovascular health of the population and to reduce the escalation of health care expenses.

Suppression of experimental atherosclerosis in rabbits by interferon-inducing agents.

The effects of two chemically different interferon inducers on the suppression of atherosclerosis were studied in rabbits fed an atherogenic chow diet. One group (10 rabbits per group) was fed normal rabbit chow, and three groups were fed an atherogenic chow. One of the latter groups received the atherogenic feeding alone; the other two were treated with either polyinosinic-polycytidylic acid (poly I:C) or 2-amino-5-bromo-6-phenyl-4-pyrimidinone (ABPP). Neither of the drugs reduced significantly the hypercholesterolemia induced by the feeding. However, both poly I:C and ABPP treatment significantly reduced the percent area of the aortic intimal surface lesions, stained for lipid with Sudan IV, compared with that in untreated rabbits fed atherogenic chow. Microscopic sections of typical aortic plaques showed that both drug treatments significantly reduced the size and number of intimal lipid deposits compared with those observed in the aortas of untreated animals. Chemical analysis for cholesterol and collagen content revealed that interferon-inducing agents significantly reduced cholesterol deposits in the aorta, with little effect on fibrous protein deposition. The results indicate that two unrelated interferon-inducing drugs suppressed atherogenesis without reducing serum cholesterol and low density lipoprotein levels. Whether the protection against atherosclerosis is exerted by endogenous interferon production remains to be determined.

Effect of high fat and high sucrose feeding on lipogenesis by isolated rat intestinal cells.

Lipid synthesis was studied in intestinal mucosal cells isolated from rats fed a high fat or a high sucrose diet. The cells actively incorporated 14C(1)-labeled free fatty acids into glycerolipids [( 1-14C]acetate was utilized for both fatty acid and cholesterol synthesis), while [14C(U)]glucose label was found in cholesterol and in the glycerol moiety of glycerolipids, but not in fatty acids. Sucrose feeding resulted in increased acetate incorporation into cholesterol, but not into fatty acids while the high fat diet markedly depressed the incorporation of acetate. In contrast, fat feeding increased both glucose and fatty acid incorporation into glycerolipids, as well as glucose incorporation into cholesterol. Using the incorporation of glucose into lipid glycerol as an estimate of the phosphatidic acid pathway, it was found that this pathway was stimulated by both fat and carbohydrate feeding. The results suggest that differences in the regulation of cholesterol and glycerolipid synthesis in the intestine compared with adipose tissue and liver may relate to the role of intestine in synthesizing lipoproteins for lipid transport.

Hyperlipoproteinemia and atherosclerosis: dietary intervention.

Elevated levels of plasma low-density lipoprotein and/or very low-density lipoprotein cholesterol, as seen in hypercholesterolemia and/or hypertriglyceridemia, are primarily caused by a diet high in saturated fat, cholesterol, and calories, and by excessive intake of alcohol. Dietary treatment constitutes the fundamental step in successful management of hyperlipidemia. An appropriately designed diet alleviates the problem to variable degrees, even in patients with primary types of hyperlipoproteinemia. Dietary therapy should be initiated when the serum cholesterol level is above 200 mg/dl in adults, and between 190 to 200 mg/dl in children, and when triglyceride values are consistently greater than 200 mg/dl. Because hyperlipidemia is often familial, due both to genetic influence and eating habits, dietary modification should be made early in life and incorporated as a permanent part of the family's life-style.

Acute myocardial infarction in patients with normal coronary arteries after acute ethanol intoxication.

Three cases are presented where acute myocardial infarction occurred in young individuals after an episode of heavy alcohol intake. Subsequent coronary arteriograms demonstrated normal coronary arteries. Several mechanisms by which acute ethanol intoxication might precipitate myocardial infarction are discussed. To our knowledge, no similar cases have been reported.