Transrectal biopsy is one of the more popular methods for the diagnosis of prostatic cancer. However, there is disagreement as to whether the use of prophylactic antimicrobials decreases the incidence of fever and urinary tract infections, which may follow this procedure. A prospective randomized double-blind study involving 63 patients was instituted to determine the efficacy of carbenicillin indanyl sodium in reducing these complications. The protocol consisted of administration of 2 tablets of 4 times daily of a placebo or the treatment drug 24 hours before and after biopsy. Clean catch urine cultures were obtained 24 hours before biopsy and at 48 hours and 2 weeks after the procedure. Blood cultures were performed 15 minutes after biopsy. In addition, clinical parameters were monitored closely in the hospital for 48 hours after biopsy. A total of 48 patients was considered evaluable. Of 23 patients who received the study drug 2 (8.6 per cent) had positive urine cultures at 48 hours compared to 9 of 25 (36 per cent) from the placebo group. A similar result was observed from the 2-week culture data, in which 2 of 23 patients (8.6 per cent) in the treatment group had positive urine cultures as opposed to 5 of 25 (20 per cent) receiving the placebo. Fever occurred in 48 per cent of the placebo and in 17 per cent of the carbenicillin groups. Our data indicate that prophylactic administration of carbenicillin indanyl sodium decreases the complications of fever and urinary tract infections following transrectal biopsy of the prostate.

The innate immune system is comprised of many components that function coordinately to prevent bacterial sepsis. However, thermal injury suppresses many of these factors, and the opportunistic pathogen Pseudomonas aeruginosa takes advantage of this condition, making it one of the leading causes of morbidity and mortality in the setting of thermal injury. P. aeruginosa is extremely efficient at colonizing burn wounds, spreading systemically, and causing sepsis, which often results in a systemic inflammatory response, multiple-organ failure, and death. The pathogenicity of P. aeruginosa is due to the arsenal of virulence factors produced by the pathogen and the immunocompromised state of the host. Syndecan 1 is a major heparan sulfate proteoglycan present on many host cells involved in thermal injury. Syndecan 1 anchored to the cell surface can be cleaved in a process termed ectodomain shedding. Syndecan 1 shedding results in the release of intact, soluble proteoglycan ectodomains that have diverse roles in innate immunity. Here we show for the first time that thermal injury results in shedding of syndecan 1 from host tissue. Our data show that syndecan 1 null mice are significantly less susceptible to P. aeruginosa infection than their wild-type counterparts, as demonstrated by (i) significantly lower mortality; (ii) absence of systemic spread of P. aeruginosa; and (iii) significant reductions in some proinflammatory cytokines. These results suggest that shed syndecan 1 plays an important role in the pathogenesis of P. aeruginosa infection of thermal injury and that syndecan 1-neutralizing agents may be effective supplements to current P. aeruginosa treatments.The gram-negative opportunistic pathogen Pseudomonas aeruginosa is particularly prevalent in burn wound infections. P. aeruginosa bacteremia is one of the leading causes of morbidity and mortality in the setting of thermal injury. It often causes multiorgan failure and results in mortality rates of up to 50% (2,25,26,39). The extensive damage induced during P. aeruginosa infection is due to the ability of the microorganism to produce a large array of virulence factors (25) and the immunocompromised state of the individual. However, the increased ability of P. aeruginosa over many other pathogens to cause sepsis in thermally injured individuals is not fully understood.

For patients with docetaxel-resistant hormone-refractory prostate cancer (HRPC) no standard chemotherapeutic treatment exists. In this study, we evaluate the efficacy of cyclophosphamide (CP)-based metronomic chemotherapy in this patient population. Patients with metastatic HRPC with disease progression under docetaxel-based chemotherapy were eligible. The primary endpoint was prostate-specific antigen (PSA) response. Secondary endpoints were survival and toxicity. Low-dose CP (50 mg/d) and dexamethasone (1 mg/d) were administered orally in a metronomic manner. Treatment was continued until disease progression or intolerable side effects occurred. Seventeen patients were enrolled in this study. The median follow-up was 12 weeks (range: 4-60). Median age was 68 years (range: 42-85). Median PSA at study entry was 134 ng/ml (range: 46.0-6554). Nine patients had a PSA response (median 44.4%), four patients >or=50% and five patients <50%. Eight patients had a PSA progression. Overall survival was 24 months. Five patients reported a decrease in bone pain after 4 weeks' treatment. No grade 3 and 4 toxicities were noted. In this study, low-dose metronomically administered CP demonstrated efficacy as a second-line treatment in patients with docetaxel-resistant HRPC. The treatment was well tolerated and almost without toxicity. Further advantages of low-dose CP were its convenient oral administration, dosing schedule, low cost, and low-toxicity profile. These attributes in combination with immunoregulatory and antiangiogenic potentials make CP also a prime candidate for combination with other treatment regimens.

These results suggest that BPH in large prostates may be protective of PCa. The interaction of the different prostate zones, in particular the transition zone and peripheral zone, may play a significant role in the phenomenon observed in this study. However, sampling error may introduce bias that 12-16 core biopsies in larger prostates may be more likely missing the cancer lesion.