Risk factors in dental implant failure

The goal of this study was to assess risk factors for dental implant failure. Eighty-three implants were placed in thirty patients who were followed for three years using digital subtraction radiography. The following putative risk factors for implant failure were employed in the model: age, sex, implant length, implant position, implant surface coating, smoking habit, and presence of infection. Implant failure was defined as progressive bone loss compromising the implant. We found that the presence of infection (P < 0.001) and absence of HA coating (P < 0.001) were the primary factors associated with early implant failure.     

Risk factors for retinopathy in diabetes mellitus in Kelantan, Malaysia

Few attempts have been made to determine the risk factors for diabetic retinopathy which is a major cause of visual impairment and blindness. One hundred and forty patients of diabetes mellitus were studied to determine the prevalence and types of retinopathy, and its relation to various risk factors. Nearly half (48.6%) of the patients suffered from retinopathy. The significant associated risk factors were long duration of diabetes, proteinuria and elevated serum creatinine level. However, there was no significant association between the prevalence of retinopathy and high levels of serum cholesterol, C-peptide levels, associated hypertension, and glycaemic control of diabetes mellitus. An effective screening programme for detection of retinopathy in the patients of diabetes as a regular practice is encouraged.     

Mechanism of activation of an N-ras oncogene of SW-1271 human lung carcinoma cells.

An N-ras-related transforming gene was detected in the human lung carcinoma cell line SW-1271 and molecularly cloned. The lesion responsible for its acquisition of transforming activity was localized to a single nucleotide transition from A to G in codon 61 of the predicted protein. This lesion in the second exon results in the substitution of arginine for glutamine at this position. These findings, together with previous studies, indicate that the activation of ras oncogenes in human tumors is most commonly due to point mutations at one of two major "hot spots" in the ras coding sequence.     

Effect of chronic tobacco-betel-lime "quid" chewing on human salivary secretions

Salivary flow rates by mechanical stimulation with forced spitting method and by chemical stimulation with 10% citric acid were determined in 25 healthy adult subjects with a history of chronic tobacco-betel-lime "quid" chewing and in 25 healthy control adults with no history of chewing. The chewers secreted more saliva as compared to nonchewers on chemical, but not on mechanical stimulation. The salivary amylase, potassium, and sodium levels were lower in chewers, but the reductions of the first two components only were significant. These reductions were thought to be due to increased salivary flow with its dilutional effect. There was no difference between the two groups with respect to salivary pH. The salivary flow rates by either method had significant positive correlation with the duration of chewing, but not with the amount of tobacco chewed. Salivary potassium was inversely correlated with the amount of tobacco chewed. It was concluded that chronic tobacco-betel-lime quid chewing induces excessive secretion of more watery saliva leading to a concomitant decrease in enzyme and electrolyte content. One or more of the following factors were considered to be operating in causing increased salivary flow in chewers effect of nicotine or tobacco on other constituents of the quid, chronic salivary gland hyperplasia, or chronic hypertrophy of the muscles of mastication.     

Histogenesis of pseudo-ductular changes induced in the pancreas of guinea pigs treated with N-methyl-N-nitrosourea

Tumors of the exocrine pancreas of the inbred strain 13 guinea pigs, induced by N-methyl-N-nitrosourea, reveal duct-like glandular differentiation and marked desmoplastic reaction of the stroma, characteristic of adenocarcinoma of human pancreas. During the course of induction of these tumors in the guinea pigs by N-methyl-N-nitrosourea, atypical pseudo-ductular proliferations were encountered in the pancreas which appeared to be precursor lesions for pancreatic carcinoma. The histogenesis of these pseudo-ductular lesions was studied by light and electron microscopy. The earliest changes consisted of dilatation of acinar lumina with decrease of apical cytoplasm and increased mitotic activity of the acinar cells. The actively proliferating, well-formed pseudo-ductules were lined by cuboidal or flattened epithelium containing a prominent nucleus and scant cytoplasm with few or no discernible zymogen granules by light microscopy. By electron microscopy, the cells lining the pseudo-ductules displayed features of immature or embryonic pancreatic acinar cells characterized by prominent nucleoli, marked decrease in rough endoplasmic reticulum with increase of free ribosomes, atypical zymogen granules and abundant microfilaments and microtubules. In two guinea pigs, transition from pseudo-ductular changes to adenocarcinoma was clearly evident. On the basis of these findings, it is proposed that the pseudo-ductular lesions of the guinea pig pancreas, and possibly those occuring in other species, are derived from acinar cells as a consequence of carcinogen induced cell proliferation leading to immature or dedifferentiated phenotypes. This hypothesis can, in part, be confirmed by immunocytochemical localization of pancreatic acinar cell specific secretory proteins and lectins in these pseudo-ductules.     

Carcinogenesis by hepatic peroxisome proliferators: evaluation of the risk of hypolipidemic drugs and industrial plasticizers to humans

In this critical review, I would like to provide a brief outline of the morphology, biochemical composition, distribution, and functions of peroxisomes. The induction of peroxisome proliferation and peroxisome-associated enzymes in the rodent liver by two classes of chemicals (hypolipidemic drugs and the industrial plasticizers) will be considered. The role of peroxisomes in lipid metabolism will be discussed. Carcinogenicity studies in rats and mice with these peroxisome proliferators will be evaluated critically. Careful consideration will be given to the hypothesis that "potent hepatic peroxisome proliferators as a class are carcinogenic." The possible mechanism(s) by which peroxisome proliferators induce liver tumors will be outlined. Particular attention will be paid to the possible role of peroxisome proliferation-mediated radical toxicity and generation of endogenous initiators of carcinogenesis.     

Effect of retinoids on the induction of colon cancer in F344 rats by N-methyl-N-nitrosourea or by 1,2-dimethyihydrazine

The possible modifying effect of synthetic and natural retinoidson the incidence of colon cancer in rats induced by 2 intrarectaldoses of 2.5 mg of N-methyl-N-nitrosourea (MNU) given once aweek for 2 successive weeks or a single 150 mg/kg body weightdose of 1,2-dime-thylhydrazine (DMH), s.c. was investigated.Emphasis was on the effect of the development of early tumorsas visualized by endoscopy. With the retinoids N-ethyl-retinamide,N-2-hydroxyethylretinamide, N-(4-hydro- xyphenyl)-all-trans-retinamide(RAHA), and retinyl acetate (RA) administered orally after thecarcinogens, significant differences in early developing tumorswere not found. At histopathological examination of the tumorsthe RAHA + DMH group had significantly fewer adenomas per animal.The percentage of adenoma bearing rats was significantly lowerin groups receiving RAHA + DMH or RA + DMH. However, food consumptionwas lower in rats consuming either RAHA or RA. Retinyl palmitate(RP) and RAHA was administered intrarectally to MNU-inducedrats either before or after the carcinogen. When administeredbefore MNU, RP caused a significant increase in the percentageof tumor bearing animals and the average number of tumors peranimal as visualized endos copically. At histopathological examination,all retinoid groups except RAHA given after the carcinogen,produced significantly more adenomas per animal and a significantlygreater adenoma incidence than did the control groups. Thus,in two systems, the oral administration of retinoids did notclearly inhibit the early or later stages of colon tumor development.Inirarectal infusion of two retinoids had no effect on colonicmor phology but at histopathological examination of later stagetumors there was an enhanced adenoma response.     

Effect of unsaturated fats and cholesterol on serum and fecal lipids. A study of healthy middle-aged men.

Modification of the Western diet, with an intake of 2,500 kcal per day and a decrease in cholesterol and fat intake to 33 per cent of calories with a P:S of 0.40, failed to alter serum lipids significantly. Evidence suggested that increasing the daily intake of cholesterol resulted in deposition in the body tissues. However, when the fatty acid composition and the P:S ratio of dietary fat were adjusted, lower serum lipids and a compensatory increase in fecal sterols occurred when cholesterol was added to the diet. Changes in serum lipoproteins in the subjects fed a "prudent" or a common diet indicate an increase in the proportion of HDL-cholesterol which may be beneficial in reducing coronary heart disease. Evidence suggests that, in absence of caloric excess, lowering of serum lipids and increased removal of fecal sterols is possible on a prudent diet without major modification of the customary foods, but that a high P:S ratio is required.     

A modified geometric factor approach to internal gamma ray dosimetry.

In internal gamma-ray dosimetry, the conventional geometric factor approach, where the "effective absorption coefficient" is taken as 0 or 0-028 cm-1, irrespective of source energy, leads to significant errors especially in the low energy region. An ettempt has been made in this paper to modify the approach to increase the accuracy of calculation and to extend its usefulness to low energies while retaining its inherent simplicity. The modification consists in replacing the effective absorption coefficient by the attenuation coefficients appropriate to the source energies and taking into account the effects due to multiple scattering by using point source build-up factor. The method has been applied for the particular case of dosimetry of a sphere. Comparison of the results obtained by this method with those got from Monte Carlo computations indicates excellent agreement at higher energies and a departure of around 15 per cent only at lower energies (as against a variation of 400 per cent when conventional geometric factor approach is used).