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Domestic violence (DV), now a national health concern, has pervasive effects at both the individual and societal levels. Women are the primary victims of DV; their lifetime prevalence has been reported to be 20%-53.8%. The sequelae of violence include increased acute and chronic health care utilization, psychological harm and a wide range of physical injuries. Head and neck injuries are the most common result of violence, and many women seek dental treatment following abuse. Dentists are in a unique position to identify abused victims and intervene. However, they are not well trained to identify victims of DV, and they lack appropriate resources to manage identified victims. Moreover, of the many health professionals surveyed, dentists feel the least responsible for intervening in cases of DV, and interventions by dentists are minimal. Barriers to screening for DV occur at the patient, provider and system levels, but they can be overcome with increased education. DV education, assessment and management should be a priority, so that dentists can help improve the lives of the many women faced with abuse.

Autoantibodies to LKM1 are present in 1 to 10% of patients with hepatitis C virus (HCV)-related chronic hepatitis (3, 4, 11, 21). The presence of these autoantibodies is associated with an increased risk of developing hepatitic flares and thyroid disorders in HCV-infected patients (17, 18). The antigenic target of anti-LKM1 antibodies is cytochrome P450IID6 (CYPIID6), a 50-kDa microsomal enzyme involved in the metabolism of xenobiotics (12, 19, 41). Molecular mimicry between HCV proteins and CYPIID6 has been suggested as a possible mechanism for the origin of these autoantibodies (2, 13). Certain HLA and CYPIID6 alleles are associated with the prevalence of LKM1 autoantibodies in some populations, suggesting the involvement of host genetic factors in the induction of these antibodies (2, 9). Immunoglobulin (Ig) GM and KM allotypes-hereditary antigenic determinants of IgG heavy chains and κ-type light chains, respectively—are associated with susceptibility to several autoimmune and infectious diseases (7, 8, 24, 27, 30, 31, 34). They also influence immune responsiveness to infectious epitopes as well as to certain autoantigens (10, 25, 26, 28, 29). Of particular relevance here, certain GM and KM determinants interact to influence the outcome of HCV infection (22). These observations led us to hypothesize that GM and KM allotypes may contribute to the generation of anti-LKM1 autoantibodies in HCV-infected subjects. Between 2002 and 2004, 129 HCV-infected patients were consecutively enrolled at the Department of Internal Medicine, Cardioangiology, and Hepatology, Alma Mater Studiorum-University of Bologna. Criteria for inclusion in the study were the following: serum anti-HCV and HCV RNA positivity, abnormal alanine transaminase levels at least twice in the past 6 months, and chronic inflammation on liver histology. Other causes of liver disease were excluded by appropriate tests. The study population also included 90 ethnically matched blood donors who were negative for anti-HCV antibodies. The study was approved by the appropriate ethics committees for human research. Anti-HCV antibodies were tested by third-generation enzyme immunoassay (Ortho HCV version 3.0 ELISA; Ortho-Clinical Diagnostics, Inc., Raritan, NJ) according to the manufacturer's instructions, and HCV RNA was tested by nested PCR using primers derived from the highly conserved 5′ noncoding region of the viral genome. Anti-LKM1 antibodies were measured by indirect immunofluorescence on cryostat sections of rat liver, kidney, and stomach specimens at a serum dilution of 1:40, and titers were determined to extinction, as previously reported (20). Serum samples were typed for G1M (1/a, 2/x, 3/f, 17/z), G2M (23/n), G3M (5/b1, 6/c3, 13/b3, 21/g), and KM 1 and 3 allotypes by a standard hemagglutination-inhibition method (38). The notation follows the international system for human gene nomenclature (35). Logistic regression and Fisher's exact test were used to determine the significance of the association between GM and KM phenotypes and the prevalence of anti-LKM1 antibodies. Odds ratios (ORs) were calculated to measure the strengths of the associations observed. ORs are not presented for comparisons where the cell counts were less than or equal to 5, as the use of large-sample theory to calculate confidence intervals for the ORs can only be justified when all of the expected cell counts are greater than 5. Statistical significance was defined as P < 0.05. Because of almost absolute linkage disequilibrium between particular GM alleles in a given race, data were analyzed as a group (phenotypes) rather than according to the presence or absence of individual markers (36). Subjects with very unusual GM phenotypes were classified as “other” for statistical analyses. All analyses were conducted using SAS version 8.1 software. The distribution of GM and KM phenotypes in relation to the presence or absence of autoantibodies to LKM1 is given in Table ​Table1.1. The GM 1,3,17 23 5,13,21 phenotype was significantly associated with the prevalence of anti-LKM1 antibodies. Its frequency was significantly higher (45%) in subjects with anti-LKM1 antibodies than in those lacking these antibodies (14%) or in random blood donors (20%; data not shown). Among HCV-infected subjects, those with GM 1,3,17 23 5,13,21 were over five times as likely to possess anti-LKM1 antibodies as those lacking this phenotype (OR = 5.13). TABLE 1. Distribution of GM and KM phenotypes in HCV-infected subjects in relation to the presence or absence of autoantibodies to LKM1 In addition to its main effect, this phenotype also interacted with the KM 1,3 phenotype (Table ​(Table2).2). Subjects with GM 1,3,17 23 5,13,21 but lacking KM 1,3, as well as those positive for both heterozygous phenotypes, were more likely to possess anti-LKM1 antibodies than those lacking both these phenotypes (P = 0.007 and 0.037, respectively). No other significant associations were found. TABLE 2. Distribution of combined GM 1,3,17 23 5,13,21 and KM 1,3 phenotypes in HCV-infected subjects in relation to the presence or absence of autoantibodies to LKM1 The results presented here show a distinct association between the presence of the heterozygous GM 1,3,17 23 5,13,21 phenotype and the prevalence of autoantibodies to LKM1. The most probable haplotypes responsible for this phenotype are GM 1,17 21 and GM 3 23 5,13. One explanation of these findings could be that the GM locus directly affects the autoreactivity to LKM1 antigens. Perhaps the B cells carrying the heterozygous phenotype GM 1,3,17 23 5,13,21 on their Ig receptors are more efficient in the uptake, processing, and subsequent presentation of LKM1 antigenic peptides to the collaborating T cells, resulting in autoantibody production. Although GM and KM markers are located in the constant region, there is a growing body of evidence for the involvement of these regions in antibody specificity usually associated with the variable (V) region of the Ig molecule. Possible mechanisms include a direct contribution to the formation of idiotypic determinants, an effect on V-region protein conformation, modulation of antibody binding affinity, and linkage disequilibrium with alleles coding for the V-region epitopes (5, 15, 16, 33, 37). The significant interaction between the GM 1,3,17 23 5,13,21 and KM 1,3 phenotypes may be a reflection of a preferential association of heavy and light chains of particular genotypes in the synthesis of LKM1 antibodies. Such nonrandom pairing of heavy and light chains has been reported for experimental animals (6, 32). It may be relevant to note that in addition to the involvement of GM and KM allotypes in the persistence and/or clearance of HCV infection mentioned earlier, we have reported interactive effects of these determinants in humoral immune responses to group B streptococcus antigens and the Epstein-Barr virus (1, 23) as well as cellular immune responses to the streptococcal cell wall antigens (39). Although statistically significant, the results of the interaction analyses should be viewed with caution. The sample size for these comparisons was small, and the findings need to be replicated in a larger study population. In addition to the direct involvement of GM and KM genes in autoreactivity to LKM1, the associations reported here could also result from linkage disequilibrium between GM and KM alleles and alleles of an as-yet-unidentified immune response gene(s) for the induction of LKM1 antibodies. Evidence for epistatic contributions of unlinked genes to the risk of human diseases is accumulating rapidly (14). In future studies, for further dissection of the associations reported here, it will be important to determine the possible interactive effects of Ig allotypes and other candidate genes on humoral and cellular immunity to the cross-reactive epitopes of HCV and CYPIID6. Among the candidate genes, HLA seems to be the most relevant, as it has been shown to be associated with the prevalence of anti-LKM1 antibodies (2). Furthermore, the simultaneous presence of particular GM and HLA phenotypes has been shown to dramatically increase (over 39 times) the risk of acquiring autoimmune chronic active hepatitis (40). KM allotypes also interact with particular HLA alleles and contribute to the occurrence of certain autoantibodies (10). To our knowledge, this is the first report of an association of GM and KM allotypes with a prevalence of anti-LKM1 antibodies.

DATA SOURCES Cochrane Oral Health Group Trials Register and the Pain, Palliative Care and Supportive Care Group Trials Register, the Cochrane Central Register of Controlled Trials, Medline and Embase. STUDY SELECTION Randomised controlled trials (RCT) were included that involved patients over the age of 18 years who had presented with a single tooth with a clinical diagnosis of irreversible pulpitis. DATA EXTRACTION AND SYNTHESIS Abstracts of studies were independently assessed by two reviewers. The primary outcome was patient-reported pain (intensity/duration) and pain relief measured on a categorical scale in the preoperative phase of irreversible pulpitis. Secondary outcomes were type, dose and frequency of medication required for pain relief. Only one trial was included so pooling of data from studies was not possible and a descriptive summary is presented. RESULTS One trial of 40 participants was included. There was a close parallel distribution of the pain ratings in both the intervention and placebo groups over the 7-day study period. The between-group differences in sum pain intensity differences for the penicillin group were 6.0+/-10.5, and for placebo 6.0+/-9.5 (P=0.776; differences assessed by Mann-Whitney-Wilcoxon test considered to be statistically significant at P=0.05). The sum pain percussion intensity differences for the penicillin group were 3.5+/-7.5 and placebo 2.0+/-7.0 (P=0.290). There was no significant difference in the mean total number of ibuprofen tablets (P=0.839) and acetaminophen tablets (P=0.325) taken for pain relief in either group over the study period. The administration of penicillin over placebo did not appear to significantly reduce the quantity of analgesic medication taken (P=0.05) for irreversible pulpitis. CONCLUSIONS This review based on one methodologically sound but low-powered small sample trial, provides some evidence that there is no significant difference in pain relief between individuals who had untreated irreversible pulpitis who did or did not take antibiotics in addition to analgesics.

Da bi obavljao posao na način stomatologije zasnovane na dokazu praktičar mora biti sposoban i pripravan oblikovati jasno pitanje, uspješno pronaći pouzdan dokaz, sustavno ispitati dokaz te, ako je važan i vjerodostojan, primijeniti rezultate procjene u svojoj praksi. Materijali, instrumenti, tehnike i terapije mijenjaju se tako brzo da mnogi od nas imaju teškoće s pamćenjem njihovih imena, a napose s pojedinostima njihove uporabe. Širenjem elektroničke tehnologije (internet, CD-ROM i DVD) znatno je lakše pronaći informacije. U mnogo slučaja pacijenti imaju isti pristup podatcima kao i liječnici, pa kako njihove razine znanja rastu, tako rastu njihova očekivanja i zahtjevi. Stomatologija zasnovana na dokazu zatvara pukotinu između kliničkog istraživanja i stvarnoga svijeta stomatološke prakse te stomatolozima daje moćne alate za interpretaciju i primjenu nalaza istraživanja. Stomatologija zasnovana na dokazu je proces koji nije rigidno metodološko ispitivanje znanstvenoga dokaza kojim se diktira što bi praktičari trebali ili ne bi trebali obavljati. U prvome redu to je proces utemeljen na integriranju znanstvene baze za kliničku skrb uporabom temeljitih, nepristranih pregleda i najpouzdanijega znanstvenoga dokaza u bilo kojem trenutku s kliničkim čimbenicima i čimbenikom pacijenta kako bi se na najbolji mogući način donijele odluke o prikladnoj zdravstvenoj skrbi za specifične kliničke okolnosti. Stomatologija zasnovana na dokazu oslanja se na ulogu pojedinačne stručne prosudbe u tome procesu., To practice in an evidence-based dentistry manner, practitioners must be able to formulate a clear question, find the best available evidence efficiently, evaluate the evidence systematically and, if it is relevant and credible, apply the results of the appraisal to their practice. Materials, instruments, techniques, and therapies change so fast that most of us have difficulty keeping up with their names, much less the details of their use. As electronic technology (Internet, CD-ROM, and DVD) expands, information retrieval is increasingly easy. Patients have access to the same data that doctors do in many cases, and as their knowledge levels increase, so do their expectations and demands. Evidence-based dentistry closes the gap between clinical research and real world dental practice and provides dentists with powerful tools to interpret and apply research findings. Evidence-based dentistry process is not a rigid methodological evaluation of scientific evidence that dictates what practitioners should or should not do. Rather, the evidencebased dentistry process is based on integrating the scientific basis for clinical care, using thorough, unbiased reviews and the best available scientific evidence at any one time, with clinical and patient factors to make the best possible decision(s) about appropriate health care for specific clinical circumstances. Evidence-based dentistry relies on the role of individual professional judgment in this process.

Purpose: To identify, classify, and evaluate agents used in the prophylaxis of oral mucositis in irradiated head and neck cancer patients. Methods: Data sources included multiple databases and manual citation review of relevant literature. Based on the eligibility criteria, 59 studies were independently reviewed by two reviewers. Forty-two studies were included in the classification scheme, of which 15 met the criteria for inclusion in the meta-analysis. Data were extracted by duplicate independent review, with disagreement resolved by consensus. Results: Overall, the interventions reduced the odds of developing severe oral mucositis, when assessed by clinicians, by 36% (OR: 0.64; 95% CI: 0.46, 0.88). Subgroup analysis suggested that only the narrow-spectrum antibacterial lozenges were effective (OR: 0.45; 95% CI: 0.23, 0.86); however, the power of the aggregated data in the other classes may have been insufficient to detect differences. When the outcome was assessed by patients, no significant difference was seen in the outcome between the treatment and the control groups (OR: 0.79; 95% CI: 0.56–1.12). Conclusions: Overall, interventions chosen on a sound biologic basis to prevent severe oral mucositis are effective. In particular, when oral mucositis is assessed by clinicians, narrow-spectrum antibiotic lozenges appear to be beneficial. Methodologic limitations were evident in many of the studies. Further research using validated measurement tools in larger, methodologically sound trials is warranted.

Carbohydrate-deficient transferrin (CDT) has been studied as an index of heavy alcohol use. The present study evaluates the utility of CDT as a marker for chronic alcohol use in medical examiner cases. Over a 5-month period, serum specimens were collected in consecutive deaths that were referred to the medical examiner's office (N = 25). Manner of death was accidental in nine cases, homicide/suicide for eight cases, and natural causes for seven cases. Fifteen of the 17 cases having alcohol abuse had positive CDT levels above threshold, indicating chronic use (sensitivity 88%). Eight cases had no evidence of alcohol abuse but three of these cases had CDT levels also above threshold (specificity 63%). There was no correlation between serum CDT levels and the time of death to blood collection for the total sample, indicating that CDT is stable postmortem for at least 36 h. CDT appears to have value as a marker of ante-mortem alcohol use prior to time of death in medical examiner cases.

Several therapies may prevent or reduce the severity of oral mucositis associated with cancer treatment

The Cornell voltage criteria and the Novacode computer model for estimating left ventricular mass were compared to echocardiographic left ventricular mass in African Americans from the Charleston Heart Study. The diagnostic accuracy of these electrocardiographic models compared with the echocardiogram is similar to the previous study in whites.

Objective The pathophysiology of pulmonary fibrosis in patients with systemic sclerosis (SSc) is poorly understood, but a number of recent studies have demonstrated an inflammatory process involving the lower respiratory tract. The objective of the present study was to determine the concentrations of several cytokines in the bronchoalveolar lavage (BAL) fluid of patients with SSc and to assess whether the enhanced expression of certain cytokines is associated with the presence of alveolitis. Methods BAL was performed on patients with SSc (with or without alveolitis) and on normal control subjects. Lyophilized BAL fluid samples were assayed by enzyme-linked immunosorbent assay for tumor necrosis factor alpha (TNF alpha), interleukin-1alpha (IL-1alpha), IL-4, IL-6, IL-8, macrophage inflammatory protein 1alpha (MIP-1alpha), and RANTES. Results There were significant differences between groups in the BAL fluid concentrations of TNF alpha (P = 0.0005, with levels in SSc patients with alveolitis higher than those in normal controls), IL-8 (P = 0.006, with levels in both SSc groups higher than those in normal controls), MIP-1alpha (P = 0.009, with levels in SSc patients with alveolitis higher than those in SSc patients without alveolitis and than those in normal controls), and RANTES (P = 0.03, with levels in SSc patients without alveolitis higher than those in normal controls). With the exception of RANTES, the highest levels were detected in SSc patients with alveolitis. Conclusion Each of these cytokines, either alone or in combination, may play an important role in the pathogenesis of pulmonary fibrosis in SSc.

Purpose To determine whether high-density lipoprotein and total cholesterol levels were risk factors for increased intraocular pressure in patients with chronic open-angle glaucoma or ocular hypertension. Methods We measured total cholesterol, high-density lipoprotein, and total cholesterol/high-density lipoprotein ratio in 25 patients with open-angle glaucoma or ocular hypertension who had taken no glaucoma medications for four weeks. We individually matched these patients to 25 control subjects who had no history of open-angle glaucoma or ocular hypertension, on the basis of age, race, gender, and history of vascular disease or diabetes mellitus. Results We found no statistical difference in the high-density lipoprotein (P = .702) or total cholesterol (P = .177) levels or total cholesterol/high-density lipoprotein ratio between groups (P = .178, paired t test). Conclusion This study indicates that increased high-density lipoprotein and total cholesterol levels are not risk factors for increased intraocular pressure.

GM and KM allotypes, powerful tools for genetic characterization of human populations, have been shown to play an important role in genetic predisposition to some infectious diseases. Two diverse racial groups--Afro-Ecuadorians and Amerindians--living in a single restricted geographical area of Ecuador, appear to have different risk factors for acquisition and clinical expression of onchocerciasis, a disease caused by the filarial parasite Onchocerca volvulus. In this study, GM and KM allotypes were determined in 25 Afro-Ecuadorians and 24 Amerindians infected with Onchocerca volvulus (INF) and in putative immune individuals (PI). In Afro-Ecuadorians, the frequency of the homozygous KM 3 phenotype was significantly decreased in INF as compared with the PI group (20 vs. 68%; P= 0.0012), while the frequency of the heterozygous KM 1,3 phenotype was increased in INF as compared with the PI subjects (48 vs. 9%; P= 0.0044). These results suggest that in Afro-Ecuadorians KM 3 is associated with a lower relative risk (resistance), whereas KM 1,3 is associated with an increased risk (susceptibility) of onchocerciasis.

Knapp RG, Schreiner PJ, Sutherland SE, Keil JE, Gilbert GE, Klein RL, Hames C, Tyroler HA. Serum lipoprotein(a) levels in elderly black and white men in the Charleston Heart Study. Clin Genet 1993: 44: 225–231. © Munksgaard, 1993 Lipoprotein(a) [Lp(a)] is an important genetic trait associated with cardiovascular disease. While Lp(a) levels have been demonstrated to be approximately twice as high in black adults and children compared with whites, this relationship has not been assessed in the elderly. During the 1987 recall of the Charleston Heart Study cohort, plasma Lp(a) [mg\dl] was measured on 113 white men and 83 black men. The average age of those having Lp(a) measurements was 71 years (\pm6) for white men and 72 years (\pm 9) for black men. The distribution of Lp(a) was skewed in both whites = (mean = 14.8, median = 8.2 mg\dl) and blacks (mean = 18.1, median = 12.8 mg/dl). The skewed distribution in elderly black men was in contrast to the bell-shaped distribution commonly reported for younger blacks. The Charleston Heart Study data suggest a shift to lower values among elderly as compared to younger men, with the greatest shift occurring among the black men. For black men who have survived to the 7th, 8th, and 9th decades of life, Lp(a) levels appear to be approaching the lower levels of white men. Despite this shift in distribution among black men, there remained a statistically significant difference in Lp(a) between racial groups.

It has been suggested that the clinical expression of autosomal dominant polycystic kidney disease (ADPKD) is uniform among individuals of a given family. To test this hypothesis, intrafamilial variations in ages at onset of first symptoms, types of first symptoms, serum creatinine concentrations, and renal sizes were evaluated in 131 patients with ADPKD from 36 unrelated families. These parameters were compared in younger and older affected relatives in the same family at a single time, due to difficulties of following them longitudinally. Because the natural course of the disease is to progress with age, it was presumed that disease progression in a given family was nonuniform if older individuals had lower serum creatinine concentrations, and/or smaller kidneys than their affected younger relatives, or if relatives of similar ages had different serum creatinine concentrations and/or kidney sizes. Nonuniform progression was suggested in 38% of affected relatives by serum creatinine concentrations and in 53% by kidney sizes. Ages at onset of first symptoms and types of first symptoms were also different in patients from the same families. These data indicate that phenotypic expression of ADPKD may differ considerably among patients who belong to the same families.

We studied 45 primary open-angle glaucoma patients consecutively examined with the program 30-2 on the Humphrey Field Analyzer to determine factors associated with a learning effect between the first two visual field exams. The average mean defect significantly decreased 1.7 dB between exams (P less than 0.05). No difference was noted in learning based on: the time interval between tests, the area of the field tested, age, sex, race, previous perimetric experience or parameters on the initial field exam (i.e. prevalence of false positive and negative errors, central reference level and eye tested (P greater than 0.05). However, learning positively correlated to defect depth and negatively correlated to fixation losses on the initial exam in patients retested within seven months (P less than 0.05). This study suggests predicting which patients require a second baseline field exam to exclude a learning effect is difficult, except in those with glaucomatous field loss or few fixation losses and another field is planned within a half year.

Background: Epidemiologic studies begun in the southeastern United States in the 1960s indicated that the prevalence of coronary disease was two to three times greater among white men than black men and also showed an excess incidence of coronary disease among white men, although hypertension was twice as prevalent among blacks. This study was conducted to determine if racial differences exist in coronary heart disease mortality and coronary risk factors. Methods: Data from the two population-based cohorts of the Charleston, SC, and Evans County, Georgia, Heart Studies were pooled to make comparisons of coronary disease mortality and its risk factors. A total of 726 black men and 1346 white men aged 35 years or older in 1960 in the combined cohort were followed up for 30 years. Results: There were 125 deaths among the black men and 323 deaths among the white men attributable to coronary disease; the age-adjusted rates were 5.0 per 1000 person-years in the black men and 6.5 per 1000 person-years in white men. Black-white coronary mortality risk ratios were 0.8 when age adjusted and 0.7 when also adjusted for other cardiovascular risk factors. Elevated systolic blood pressure and cigarette smoking were significant predictors of coronary mortality in black and white men. Serum total cholesterol level was a statistically significant risk factor only in white men. Higher education level was significantly protective in black and white men. Conclusions: Black men experienced significantly less coronary disease mortality than white men. Except for cholesterol level, the risk factors for coronary mortality in black and white men were similar. (Arch Intern Med. 1995;155:1521-1527)

• With the use of photon absorptiometry, bone mineralization was measured at birth and 8 and 16 weeks after delivery in 12 very-low-birth-weight premature (mean ± SD gestational age, 31 ±1.5 weeks) infants who required minimal medical support. Simultaneously, 19 healthy term infants were studied. Throughout the study, each neonate received modified 84–kJ/30 mL formula containing no added calciferol. The recommended daily allowance (400 IU) of calciferol was given to each infant as an oral supplement. Serum 25-hydroxyvitamin D, calcium, phosphorus, and parathyroid hormone concentrations were monitored biweekly and were normal. Bone mineral content and bone width significantly differed at birth between the term and premature infants. However, by 16 weeks after delivery, the premature infants had exceeded the bone mineral status of the term infants at birth, and their bone mineral content was not significantly lower than that of the term infants. These data indicate improved bone mineralization as compared with previously reported data from very-low-birth-weight neonates. ( AJDC . 1990;144:36-40)

During the 1984/1985 recall of the Charleston Heart Study Cohort, physical function data were obtained for 247 white males, 376 white females, 123 black males, 247 black females and 71 high socioeconomic status (SES) black males over 60 years of age. Black females had the highest prevalence of physical disability (55.8%), followed by white females (43.2%), black males (39.0%) and white males (25.8%) and high SES black males (22.3%). Physical disability was 1.5–2.5 times as prevalent among individuals with a history of cardiovascular disease (CVD) than those without such a history. Among individuals without a current history of CVD univariate analyses showed the following as significant (lower 95% CI > 1.0) predictors of physical disability: elevated systolic blood pressure in white females, black males, and black females; elevated cholesterol in black females; obesity in black females; and low educational level in white females. Regression analyses indicated that obesity in 1960 accounted for 10.9 and 2.9% respectively of the variability in physical disability scores in 1985 for black females and white females.

Renal kallikrein responses to dietary protein: A possible mediator of hyperfiltration. We studied GFR, RPF and renal kallikrein in rats fed 9%, 25%, or 50% protein (casein) diets for 8 to 13 days. GFR and RPF increased progressively with increasing dietary protein. Renal excretion of active kallikrein (µg/day) was 128 ± 9, 174 ± 11 and 228 ± 14 in 9%, 25%, and 50% protein-fed rats, respectively (P < 0.02 or less between groups). Prokallikrein excretion in these groups was 23 ± 7, 77 ± 11 and 118 ± 15 µg/day, respectively (P < 0.005 or less between groups). The in vivo renal kallikrein synthesis rate, relative to total protein synthesis, was reduced in 9% protein-fed rats (2.74 ± 0.24) compared to rats fed 25% (3.93 ± 0.34, P < 0.02) or 50% protein (4.41 ± 0.30, P < 0.001). These changes in synthesis and excretion rates were not accompanied by changes in renal tissue levels of active or prokallikrein. In all groups, GFR and RPF correlated directly with the renal excretion of active kallikrein, prokallikrein or total kallikrein (r = 0.41 to 0.66, P < 0.01). Treatment of 50% protein-fed rats with aprotinin, a kallikrein inhibitor, markedly lowered renal and urinary kallikrein-like esterase activity. Left kidney GFR and RPF were significantly reduced in aprotinin-treated rats compared to vehicle-treated rats (1.54 ± 0.15 and 4.86 ± 0.38 ml/min vs. 1.89 ± 0.10 and 5.93 ± 0.22 ml/min, GFR and RPF, respectively, P < 0.05 or less). Protein-induced changes in renal kallikrein synthesis and excretion could not be explained by changes in aldosterone excretion, plasma renin activity, or electrolyte and water intake or excretion. The data suggest that renal kallikrein and kinins participate in mediating the renal vasodilatory effect of dietary protein.

We have conducted a controlled trial on the efficacy of cyclosporine in eight patients with steroid-resistant nephrotic syndrome (four with idiopathic minimal lesion nephrotic syndrome and four with focal segmental glomerulosclerosis). Patients were randomly allocated to a cyclosporine (5 mg/kg/d) or a control group. After eight weeks of therapy and one month without cyclosporine therapy, patients in the control group were given cyclosporine for eight weeks and those in the cyclosporine group became controls. Before the initiation of treatment, there was no difference between the groups with regard to proteinuria and serum albumin levels. Proteinuria remained unchanged in the cyclosporine group, while there was a significant increase in proteinuria in the control group. There were no significant changes in serum albumin levels in either group during the trial. This study does not support the use of cyclosporine at the dose of 5 mg/kg/d in patients with steroid-resistant minimal lesion nephrotic syndrome or focal segmental glomerulosclerosis.

Background In the United States, life expectancy is significantly lower among blacks than whites. We examined whether socioeconomic status (SES) and cardiovascular disease (CVD) risk factors may help explain this disparity. Methods Forty years (1961 through 2000) of all-cause mortality data were obtained on a population-based cohort of 2,283 subjects in the Charleston Heart Study (CHS). We examined the influence of SES and CVD risk factors on all-cause mortality. Results Complete data were available on 98% of the original sample (647 white men, 728 white women, 423 black men, and 443 black women). After adjusting for SES and CVD risk factors, the hazard ratios (HRs) for white ethnicity were 1.14 (0.98 to 1.32) among men and 0.90 (0.75 to 1.08) among women, indicating that the mortality risk was 14% greater for white men and 10% lower for white women compared to their black counterparts. However the differences were not statistically significant. Conclusion While there are marked contrasts in mortality among blacks and whites in the CHS, the differences can be largely explained by SES and CVD risk factors. Continued focus on improving and controlling cardiovascular disease risk factors may reduce ethnic disparities in survival.