First‐degree relatives (FDRs) of patients with colorectal cancer (CRC) have an increased CRC risk. Few studies have addressed if adenoma and advanced adenoma risk is increased among individuals, 40–49 years of age, with a family history of CRC. Therefore, the aim of the study was to define the prevalence and location of adenoma, advanced adenoma and CRC, according to age, in asymptomatic individuals with a family history of CRC.

Although several studies have shown that chlorhexidine digluconate (CHX) has bactericidal activity against periodontal pathogens and exerts toxic effects on periodontal tissues, few have been directed to evaluate the mechanisms underlying its adverse effects on these tissues. Therefore, the aim of the present study was to investigate the in vitro cytotoxicity of CHX on cells that could represent common targets for its action in the surgical procedures for the treatment of periodontitis and peri-implantitis and to elucidate its mechanisms of action. Osteoblastic, endothelial and fibroblastic cell lines were exposed to various concentrations of CHX for different times and assayed for cell viability and cell death. Also analysis of mitochondrial membrane potential, intracellular Ca2+ mobilization and reactive oxygen species (ROS) generation were done in parallel, to correlate CHX-induced cell damage with alterations in key parameters of cell homeostasis. CHX affected cell viability in a dose and time-dependent manners, particularly in osteoblasts. Its toxic effect consisted in the induction of apoptotic and autophagic/necrotic cell deaths and involved disturbance of mitochondrial function, intracellular Ca2+ increase and oxidative stress. These data suggest that CHX is highly cytotoxic in vitro and invite to a more cautioned use of the antiseptic in the oral surgical procedures.

Age and sex differences in the incidence of gastrointestinal cancers suggest the involvement of sex steroids. Post-menopausal loss of estrogen in women appears to be associated with a lower risk of colonic cancer, and studies in vitro have shown that estradiol (E2) stimulates the growth of colonic cancer cell lines. Paradoxically more recent epidemiological data have shown that hormone replacement therapy (HRT) is associated with a lower risk of colonic cancer, although this may reflect differences in the composition and route of administration of HRT regimes. The precise mechanism by which estrogens influence colonic cancer in vivo remains unclear, although E2-induced growth of colonic cancer cells in vitro appears to be dependent on estrogen receptor (ER) expression. We have previously demonstrated differential responses to E2 in pre-malignant and malignant colonic cancer cell lines, without any apparent difference in ER expression. Analogous to well documented studies in breast cancer, we have postulated that local steroid metabolism in the colon may play a key role in modulating the effects of oestrogens by determining the tissue availability of active E2. Using biopsy material we have shown that the normal colonic mucosa has a high level of 17β-hydroxysteroid dehydrogenase (17β-HSD)-mediated E2 metabolism. Furthermore, the predominant enzyme activity, inactivation of E2 to estrone (E1), was significantly decreased in paired tumor biopsies. The presence of 17β-HSD activity in the colon appears to be due to expression of the type 2 and 4 isozymes of 17β-HSD (17β-HSD2 and 4), and expression of mRNA for the latter was shown to be significantly decreased in tumours compared to normal mucosa. Further studies have characterised the expression of 17β-HSD2 and 4 in colonic epithelial cells and in colonic cancer cell lines, and have suggested a link between estrogen metabolism and colonic cell proliferation. Data reviewed here provide evidence for the importance of 17β-HSD isozymes as attenuators of E2 bioavailability in the colon, and emphasise a possible role for 17β-HSD2 and 4 in the pathogenesis of colon cancer.

ethods: 20 consecutive patient undergoing TKA, 14 females and males were given the following anesthetic protocol: continuous emoral nerve block obturator nerve block (both branches) ateral femoral cutaneous nerve block parasacral sciatic nerve lock. As local anestetic(LA) a total volume of 50 ml mixture of opivacaine 0.75% and mepivacaine 1.5% in equal parts was given. ll blocks were performed under US guidance at the most proximal evel, and optimizing LA volume. (Electrical stimulation was not sed). A observer blind to the anesthesia technique evaluated 1) utaneous area of analgesia, 2) motor block, 3) surgical anesthesia, ) need for iv analgesic supplementation, 5) postoperative analgeia, 6) patient acceptance and satisfaction, 7)surgeon satisfaction. lso were recorded acute or delayed comlications related to the erve nlockade.

BACKGROUND AND OBJECTIVES:This prospective randomized controlled trial investigated the clinical efficacy of stimulating catheters for continuous femoral nerve block in patients who underwent anterior cruciate ligament reconstruction. METHODS:Seventy patients were randomized to either a stimulating catheter (SC, n = 35) or a nonstimulating catheter (NSC, n = 35) for femoral nerve block using 25 mL ropivacaine 7.5 mg/mL and clonidine 50 microg injected through the catheter. A single-injection sciatic block was also given to ensure surgical anesthesia. The time to loss of sensation to cold and pinprick of the femoral nerve was registered as the onset time. Data were registered intra- and postoperatively regarding pain scores, adverse effects, and need for supplemental anesthesia and analgesia other than a continuous postoperative infusion of ropivacaine 2 mg/mL through the continuous femoral nerve catheter set at 7 mL/h. RESULTS:Onset time was faster in the SC group (SC: 6.4 +/- 2.5, NSC: 8.3 +/- 2.9 min, P = .006). Visual analog scale pain scores were similar in both groups. The number of patient-controlled regional analgesia boluses (SC: 14.6 +/- 12.6, NSC: 23.2 +/- 13.6 mg ropivacaine 2 mg/mL, P = .008) as well as intravenous rescue ketorolac (SC: 34.3 +/- 35.7, NSC: 54 +/- 39.7 mg, P = .033) administered were higher in the NSC group. CONCLUSION:Although the use of a stimulating catheter was associated with faster onset time for the femoral nerve block and lower additional analgesics postoperatively, the clinical superiority (analgesia; lateral femoral cutaneous, and obturator nerve block) of stimulating catheters was not evident in this clinical setting.

Survival and prognostic factors of all the patients (pts) presenting at Pistoia Hospital General Surgery between January 1990 and December 2000 are compared to those reported in the literature. Clinico-pathological indicators, the timing of admission, the surgeon's experience and the ward where the pts were cured were all evaluated. The operative mortality was 8.1%. Five-year survival was 41.3%. When a statistical analysis was performed, an age > 70 years, serosal invasion, resection-line involvement, LN ratio > 20% and the ward were independent prognostic factors. In a secondary care hospital, outcome parameters are similar to those reported by most authors. Nevertheless the prognostic effect of the surgeon's experience and perioperative treatment must be stressed.

The effect of ipriflavone (IP), a synthetic isoflavonoid derivative, on in vivo bone formation was studied in rat perialveolar bone by surgically producing a hole in the mandibular bone. The holes were filled either with powdered IP or with compounds containing no osteoinductive properties such as biostite and Htr (hard tissue replacement). In control animals, the holes were left to heal spontaneously. The animals were killed 3, 28, and 40 days after surgery and a detailed morphological and morphometric study was performed on the perialveolar bone surrounding the wounds. Three days after surgery (inflammatory phase) the bone wounds were occupied by hemorragic and inflammatory cells in both the untreated and IP-treated bone defects. Twenty-eight days after surgery, bone formation was evident with new bone spiculae particularly concentrated in the area of the bone lesion closest to the adjacent periodontal ligament. Morphometric measurements of the areas occupied by new bone showed that the synthesis of perialveolar bone was significantly stimulated by IP. The repair of the bone defects by new bone formation progressed by day 40, but only in the presence of IP were the original holes almost completely repaired. Conversely, biostite and Htr did not influence promotion of new bone formation. In conclusion, the results of the present study are consistent with a role of IP in stimulating osteogenesis and suggest that this compound could represent a potential therapeutic tool to promote repair of injured perialveolar bone.