Background and aim-Chronic idiopathic intestinal pseudo-obstruction (CIIP) is characterised by severe impairment of intestinal propulsive motility that mimics bowel obstruction. JC virus (JCV) is a polyomavirus that can infect brain glial cells causing a fatal disease, but may also be found throughout the normal gastrointestinal tract. The hypothesis that JCV infects the myenteric plexuses of patients with CIIP was tested.
Purpose: Liver transplant recepients (LTRs) have an increased risk of colorectal neoplasia. The mechanism responsible for this is unknown. JCV encodes for TAg and has been implicated in colorectal carcinogenesis.We hypothesized that the use of immunosuppression in LTRs facilitates activation of JCV and is responsible for the increased risk of neoplasia. Experimental Design: JCV TAg DNA and protein expression were determined in normal colonic epithelium (n = 15) and adenomatous polyps (n = 26) from LTRs and compared with tissue samples from control patients (normal colon, n = 21; adenomas, n = 40). Apoptosis and proliferation were determined by M30 and Ki-67 immunoreactivity, respectively. Results: JCV TAg DNA was found in 10 of 15 (67%) of normal colonic mucosa from LTRs compared with 5 of 21 (24%) of control normal mucosa (P = 0.025). JCV TAg DNA was detected in 16 of 26 (62%) of the adenomas from LTRs and in 20 of 40 (50%) of control adenomas. JCV TAg protein was expressed in 13 of 26 (50%) adenomas from LTRs versus 2 of 40 (5%) of adenomas from controls (P < 0.001). In adenomas from LTRs, the mean proliferative activity was higher compared with controls (60.3 F 3.2 % versus 42.7 F 2.8 %, P < 0.001), whereas mean apoptotic indices were lower in LTRs (0.29 F 0.08% versus 0.39 F 0.06%, P = 0.05).
Conclusions:The presence of JCV in the colorectal mucosa and adenomas from LTRs, in concert with the use of immunosuppressive agents, suggests thatJCV may undergo reactivation, and the subsequent TAg protein expression might explain the increased risk of colorectal neoplasia in LTRs.
Summary:Healthy stem cell donors start leukapheresis 4-5 days after starting G-CSF based on the peripheral blood CD34 þ cell count (PBCD34). Data from 137 harvests (68 donors) were analyzed to determine correlation between pre-apheresis leukocytes (11.0-94.8 Â 10 9 /l; median 38.8) and platelets (49-374 Â 10 9 /l; median 180), and PBCD34 (3-276/ll; median 40). PBCD34 correlated positively with leukocytes (r ¼ 0.48; Po0.0001) and platelets (r ¼ 0.40; Po0.0001). When pre-apheresis leukocytes were X25 and platelets were X100, PBCD34 and CD34 þ collection were 5-276/ll (median 57) and 0.5-27.6 Â 10 6 /kg (median 4.7), respectively; significantly higher than PBCD34 of 3-74/ll (median 17) and CD34 þ collection of 0.2-8.9 Â 10 6 /kg (median 2.2) when leukocytes were o25 and/or platelets were o100. With leukocytes X25 and platelets X100, PBCD34 was low (o20/ll) 8% of the time, compared to 57% of the time with leukocytes o25 and/or platelets o100 (Po0.0001). Our data suggest that it is not always necessary to measure PBCD34 to guide leukapheresis in healthy donors because pre-apheresis leukocytes and platelets X25 and X100, respectively, are associated with excellent mobilization. When blood counts do not meet these criteria, PBCD34 should be determined prior to initiation of apheresis.
Approximately 60% of deaths in patients with AIDS are a direct result of infection other than HIV. The more severe and life-threatening complications of HIV infection occur in patients with a CD4(+) T cell count <200 cells/μL. In the absence of effective retroviral therapy, these infections are associated with a high mortality. We describe a case of disseminated toxoplasmosis discovered at autopsy in a patient with undiagnosed AIDS.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.