Resistance of O-acetylated gonococcal peptidoglycan to human peptidoglycan-degrading enzymes.

Two naturally occurring forms of gonococcal peptidoglycan (PG) were tested for their susceptibility to human PG hydrolases. Purified 3H-labeled PG substituted extensively with O-acetyl derivatives (O-PG; from Neisseria gonorrhoeae FA19) and 14C-labeled O-acetyl-deficient PG (non-O-PG; from N. gonorrhoeae RD5) were mixed together and treated with either normal human sera (NHS) or with lysozyme purified from human polymorphonuclear leukocytes (PMN-LZ). The initial rate of hydrolysis of O-PG by NHS or by PMN-LZ was two- to fourfold less than that of its non-O-PG counterpart in the same tube. When the reactions were allowed to go to completion. NHS solubilized both PGs completely, whereas PMN-LZ solubilized all of the non-O-PG and left ca. 60% of the O-PG insoluble. The PMN-LZ-soluble fraction of O-PG consisted largely of glycosidically linked fragments with molecular weights greater than ca. 10(4), whereas the corresponding non-O-PG was degraded to lower-molecular-weight fragments, exclusively. At completion, NHS hydrolyzed both PGs to fragments whose size was equal to or smaller than that of the free disaccharide unit of PG, suggesting that human sera contain a peptide-splitting (amidase) activity and a glycosidase activity, in addition to that of the well-known muramidase. NHS also promoted the release of high-molecular-weight PG fragments from intact gonococci. The persistence of human hydrolase-resistant PG in the form of soluble macromolecular fragments may potentiate the biological effects of gonococcal PG in vivo.     

3,3',4,4'-Tetrabromobiphenyl sensitizes rats to the hepatotoxic effects of endotoxin by a mechanism that involves more than tumor necrosis factor.

To determine whether the cytokine tumor necrosis factor/cachectin might be a mediator of hepatotoxicity seen after exposure to polyhalogenated aromatic hydrocarbons, rats treated with a single dose of 3,3',4,4'-tetrabromobiphenyl (150 mumol/kg intraperitoneally) or corn oil vehicle were studied. The 3,3',4,4'-tetrabromobiphenyl caused the expected anorexia, alterations in organ weights and changes in cytochromes P-450 over 21 days. Although tumor necrosis factor could not be detected in the serum of rats at any time after 3,3',4,4'-tetrabromobiphenyl treatment alone (from 90 min to 21 days), 3,3',4,4'-tetrabromobiphenyl treatment significantly increased peak serum tumor necrosis factor concentrations after intravenous bacterial endotoxin (lipopolysaccharide, 1 mg/kg). This effect was seen with lipopolysaccharide given 24 hr, 48 hr, and 20 days after 3,3',4,4'-tetrabromobiphenyl treatment and increases in peak serum tumor necrosis factor levels ranged from threefold to eightfold over controls in various experiments with no significant differences between the three time points. However, a synergistic increase in hepatic damage (assessed by serum enzymes and liver histological findings 24 hr after lipopolysaccharide injection) was seen in rats given lipopolysaccharide 24 hr and 48 hr after 3,3',4,4'-tetrabromobiphenyl administration, with 75% and 25% lethality, respectively. There was no lethality with lipopolysaccharide given 20 days after 3,3',4,4'-tetrabromobiphenyl administration or with simultaneous administration. A lower dose of lipopolysaccharide (0.1 mg/kg) given 24 hr after 3,3',4,4'-tetrabromobiphenyl also enhanced hepatotoxicity and serum tumor necrosis factor but without lethality. Lipopolysaccharide decreased cytochromes P-450 concentrations and activities to similar extents at all time points tested in both control and 3,3'4,4'-tetrabromobiphenyl-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term Allograft Survival After Kidney Transplantation

BackgroundTechnical and medical advances over the past few years have produced an important increase in the functionality of renal allografts. The aim of this study was to identify the factors associated with allograft survival 15 years after transplantation in our series.MethodsA retrospective study of kidney transplantations was carried out at Reina Sofia Hospital in Cordoba from February 1979 to December 1997, with follow-up through June 2012. A subanalysis of the series was undertaken, and Kaplan-Meier analysis and Cox proportional hazards model regression used to achieve the main objective of the study.ResultsA total of 487 renal allografts with a mean follow-up of 114 months were studied, of which 37% (n = 180) survived for >15 years. Of the 180 patients, the main causes of graft failure were chronic allograft nephropathy in 29 (66%) and patient death in 13 (29.5%). Multivariate analysis identified the number of HLA mismatches (hazard ratio [HR] 1.25, 95% CI 1.01–1.56), panel reactive antibodies (HR 2.61, 95% CI 1.28–5.26), and delayed graft function (HR 11.25, 95% CI 1.33–95.28) as being significantly associated with graft loss after 15 years.ConclusionsThe high immunologic risk of the patients was independently associated with graft loss. Delayed graft function was the most important factor in the speed of graft failure beyond 15 years.     

Opciones de tratamiento quirúrgico en la estenosis de uretra bulbar

ObjectiveTo review the outcome of bulbar urethroplasty using two stage surgical techniques.Material and methodsTwenty-two of the 35 patients studied corresponded to end-to-end urethroplasty (ATT) and 13 to dorsal onlay graft (DOG) in preputial skin or oral mucosa variants. Clinical outcome was considered a failure when postoperative surgery was needed or the uroflowmetry was less than 15 ml/s. The following variables were studied: age, previous surgery, number of urethrotomies and stricture length. The curves and log-rank Curves using the log-rank were elaborated for follow-up and comparison, with the Cox regression model for risk factors.ResultsMean follow-up was 40.02 months. Of all the cases. 85.71% were successful. Of these, 86.36% were in the ATT group and 84.61% in the DOG group. There were no significant differences in the comparative LR test based in stricture length, previous surgery between both group and individualized for each management. The Cox regression model showed a risk of failure in the technique for the elderly patients (OR 2.2), it not achieving statistical significance in the remaining variables.ConclusionsThe success rate achieved with the ATT technique is verified a gold standard option in short strictures. The DOG is shown as a valid option in long strictures in bulbar urethral in medium follow-up, using a oral mucosa or preputial onlay graft. More long-term follow-up must be performed with a greater number of patients to better evaluate these results.     

Classification and management of rectal prolapse after anorectoplasty for anorectal malformations

Purpose

To suggest a classification, describe the risk factors and management of rectal prolapse after anorectoplasty for anorectal malformations (ARMs).

Methods

We classified prolapse as minimal (rectal mucosa visible with Valsalva manoeuvre), moderate (prolapse <5 mm without Valsalva), evident (>5 mm without Valsalva) and compared patients with and without prolapse within our ARM-population.

Results

Among 150 patients, 40 (27 %) developed prolapse: 25 minimal, 6 moderate, 9 evident. Prolapse affected 33 % of males (9 % of perineal fistulas, 38 % of bulbar, 71 % of prostatic, 60 % of bladder neck and 13 % without fistula) and 21 % of females (9 % of perineal, 30 % of vestibular, 50 % of cloacas, and 25 % without fistula). Risk factors for prolapse were: tethered cord (40 vs 24 %), vertebral anomalies (39 vs 24 %), laparoscopic-assisted anorectoplasty (LAARP) (75 vs 25 %), and colostomy at birth (49 vs 9 %). Redo anorectoplasty was not associated with prolapse. Symptoms were present in 11 patients (28 %): in 7 % with minimal, 33 % with moderate and 77 % with evident prolapse. Nine patients (2 moderate, 7 evident) underwent surgical correction.

Conclusion

Severe ARMs, tethered cord, vertebral anomalies, colostomy, and LAARP predispose to rectal prolapse. Classifying prolapse allows to predict symptoms and need for surgical correction, and to compare outcomes among different centers.     

Reference values for the echocardiographic calculation of left ventricular mass in normal children between the ages of 0 and 6]

BACKGROUND. Echocardiographic assessment of left ventricular mass (LVM) and mass/volume ratio (LVM/V) is an accurate method for evaluating left ventricular hypertrophy. However, reference values for LVM and left ventricular volume (V) in children under 6 years of age have not been well established. METHODS. Therefore, we evaluated 106 consecutive children (60 males, 46 females, mean age +/- SD 35 +/- 28 months, range 0-72) free of cardiovascular disease by clinical, electrocardiographic and echocardiographic examination. LVM and V were determined by M-mode echocardiography. RESULTS. The 5th and 95th percentile values of LVM were: 7 and 21 grams for infants aged 0 to 6 months; 13 and 32 grams for 7 to 24 months; 23 and 41 grams for 25 to 36 months; 23 and 59 grams for 37 to 48 months; 30 and 60 grams for 49 and 60 months; 36 and 98 grams for 61 and 72 months. The 5th and 95th percentile values of V were: 4 and 20 ml for infants aged 0 to 6 months; 12 and 36 ml for 7 to 24 months; 16 and 43 ml for 25 to 36 months; 20 to 55 ml for 37 to 48 months; 27 to 64 ml for 49 to 60 months; 39 to 74 ml for 61 to 72 months. The 5th and 95th percentile values of M/V ranged between 1 and 2.3 for infants aged 0 to 6 months, and 0.7-1.2 for those aged 61 to 72 months. LVM, V and LVM/V were significantly (p < 0.0001) related to age, height, weight and body surface area, but were unrelated to gender.     

Estrogen induced growth of human breast cancer cells (MCF-7) in athymic nude mice is enhanced by secretions from a transplantable pituitary tumor

MCF-7, a human breast carcinoma cell line, was maintained s.c. in female athymic nude mice for a period of 5–6 weeks. Administration of estrogen (s.c. pellet of 17β-estradiol and estrone in drinking water, 0.5 mg/l) to these mice resulted in sustained (P < 0.001) growth of MCF-7 tumors. Grafting of a prolactin and growth hormone secreting rat pituitary tumor to the estrogen-treated mice resulted in an increased (P < 0.05) rate of MCF-7 tumor growth. MCF-7 did not grow in athymic nude mice grafted with rat pituitary tumor alone or in mice without hormone treatment (controls). Thus, secretions of pituitary hormones alone are not capable of promoting in vivo growth of MCF-7 although such secretions significantly enhance estrogen-induced growth of this cell line. A synergism between pituitary hormones and estrogen for in vivo growth of a human breast carcinoma has been demonstrated in this study.