Activated duodenal mucosal eosinophils in children with dyspepsia: a pilot transmission electron microscopic study.

Background: Activated eosinophils can be identified by electron microscopy (EM) Previous studies have shown EM evidence of eosinophil activation in a variety of gastrointestinal conditions associated with inflammation. The purpose of this study was to evaluate the activation state by EM of duodenal mucosal eosinophils in children who presented with dyspepsia and to determine if eosinophils are activated in patients with normal eosinophil counts on routine histology.

Methods: Twenty patients (ages 7-15 years) with dyspepsia were evaluated.

Reversible stress relaxation during precoalescence interruptions of volmer-weber thin film growth.

From in situ stress measurements, we have observed that a large component of the precoalescence compressive stress that develops during Volmer-Weber growth of polycrystalline Cu films relaxes reversibly. This phenomenon is similar to the reversible stress relaxation previously observed in the postcoalescence regime. We have also observed that less than a tenth of a monolayer of deposition leads to an instantaneous stress of order 1 GPa.

Sexual orientation and height, weight, and age of puberty: new tests from a British national probability sample.

Research using non-representative samples indicates that certain sex-dimorphic physical, developmental and behavioral variables predict sexual orientation. In this study, three sex-dimorphic physical development variables-height, weight, and age of puberty/sexual maturation-and sexual orientation were examined in a British national probability sample (N=18,876). Women with same-sex inclinations (particularly bisexuals) had an earlier first sexual experience (approx.

Age of puberty and sexual orientation in a national probability sample.

The relations between sexual orientation and age of puberty in both men and women were examined in a national probability sample of the United States. The sample was the National Health and Social Life Survey (E. O.

Activation of apoptosis pathways in peripheral blood lymphocytes by in vivo chemotherapy.

In addition to myelosuppression, anticancer drugs cause rapid and persistent depletion of lymphocytes, possibly by direct apoptosis induction in mature T and B cells. Induction of apoptosis regulators was analyzed in peripheral blood lymphocytes from pediatric patients undergoing first-cycle chemotherapy for solid tumors. In vivo chemotherapy induced a significant increase in lymphocyte apoptosis ex vivo.

Cell type specific involvement of death receptor and mitochondrial pathways in drug-induced apoptosis.

Apoptosis in response to cellular stress such as treatment with cytotoxic drugs is mediated by effector caspases (caspase-3) which can be activated by different initiator pathways. Here, we report on a cell type specific triggering of death receptor and/or mitochondrial pathways upon drug treatment. In type I cells (BJAB), both the receptor and the mitochondrial pathway were activated upon drug treatment, since blockade of either the receptor pathway by overexpression of dominant negative FADD (FADD-DN) or of the mitochondrial pathway by overexpression of Bcl-X(L) only partially inhibited apoptosis.

Reflexive joint attention depends on lateralized cortical connections.

Joint attention, the tendency to spontaneously direct attention to where someone else is looking, has been thought to occur because eye direction provides a reliable cue to the presence of important events in the environment. We have discovered, however, that adults will shift their attention to where a schematic face is looking--even when gaze direction does not predict any events in the environment. Research with 2 split-brain patients revealed that this reflexive joint attention is lateralized to a single hemisphere.

Cytotoxic drugs and the CD95 pathway.

Cytotoxic drugs commonly used in chemotherapy of leukemia and solid tumors have been shown to primarily act by inducing apoptosis in sensitive target cells. Apoptosis may involve activation of death-inducing ligand/receptor systems such as CD95 (APO-1/Fas). Treatment with anticancer drugs such as doxorubicin, methotrexate, cytarabine, etoposide and cisplatin at therapeutic concentrations leads to induction of CD95-ligand (CD95-L).

Induction of CD95 ligand and apoptosis by doxorubicin is modulated by the redox state in chemosensitive- and drug-resistant tumor cells.

Induction of CD95 ligand (CD95-L) may contribute to drug-induced apoptosis in chemosensitive leukemias and solid tumors. Here we report that induction of CD95-L and apoptosis by doxorubicin in leukemic and neuroblastoma cells is regulated by the redox state and reactive oxygen species (ROS). Preincubation of chemosensitive cells with antioxidants such as N-acetyl-cysteine (NAC) or glutathione (GSH), significantly reduced doxorubicin-induced apoptosis, hyperexpression of ROS, loss of mitochondrial membrane potential (DeltaPsim) and upregulation of CD95-L expression.

Decreased sensitivity of drug-resistant cells towards T cell cytotoxicity.

Killing of target cells by cytotoxic T cells is mediated by induction of apoptosis requiring functional death pathways. Kill is mediated either by the CD95 or the perforin/granzyme pathway. We found that SH-EP neuroblastoma cells are preferentially killed via CD95, while in the T leukemia cell line CEM CD95 and perforin/granzyme are involved.

Chemotherapeutic drugs sensitize pre-B ALL cells for CD95- and cytotoxic T-lymphocyte-mediated apoptosis.

The CD95 (APO-1/Fas) system plays an important role in lymphocyte homeostasis and contributes to anticancer drug-induced apoptosis in some tumor cells. Most childhood B-lineage ALL cells are constitutively resistant towards CD95-induced death. We report here that chemotherapeutic drugs, such as doxorubicin, cytarabine, methotrexate and 6-mercaptopurine, sensitize CD95-resistant pre-B-ALL cell lines for CD95- and lymphokine-activated killer (LAK)-induced cell death.

Lactation duration: influences of human milk replacements and formula samples on women planning postpartum employment.

Objective: To examine the influences of inhospital administration of breast milk replacements and receipt of formula samples on lactation duration among women planning postpartum employment.

Design: Prospective design.

Setting: Telephone interviews conducted prenatally and at 6 weeks, 3 months, and 6 months post-partum.

Molecular determinants of apoptosis induced by cytotoxic drugs.

Recent experimental evidence suggests that apoptosis pathways such as the CD95 system are an important mediator of chemotherapy-induced apoptosis in various tumor cell lines. Therapeutic concentrations of cytotoxic drugs induce CD95 and CD95-L that mediates apoptosis via an autocrine/paracrine loop by crosslinking CD95. Interfering with CD95-L/receptor interaction by antagonistic antibodies to the receptor or by inhibition of CD95-L expression strongly reduces apoptosis.

Two CD95 (APO-1/Fas) signaling pathways.

We have identified two cell types, each using almost exclusively one of two different CD95 (APO-1/Fas) signaling pathways. In type I cells, caspase-8 was activated within seconds and caspase-3 within 30 min of receptor engagement, whereas in type II cells cleavage of both caspases was delayed for approximately 60 min. However, both type I and type II cells showed similar kinetics of CD95-mediated apoptosis and loss of mitochondrial transmembrane potential (DeltaPsim).

Chemosensitivity of solid tumor cells in vitro is related to activation of the CD95 system.

We have identified the CD95 system as a key mediator of chemotherapy-induced apoptosis in leukemia and neuroblastoma cells. Here, we report that sensitivity of various solid tumor cell lines for drug-induced cell death corresponds to activation of the CD95 system. Upon drug treatment, strong induction of CD95 ligand (CD95-L) and caspase activity were found in chemosensitive tumor cells (Hodgkin, Ewing's sarcoma, colon carcinoma and small cell lung carcinoma) but not in tumor cells which responded poorly to drug treatment (breast carcinoma and renal cell carcinoma).

Deficient activation of the CD95 (APO-1/Fas) system in drug-resistant cells.

The molecular mechanisms for sensitivity and resistance of tumor cells towards chemotherapy are only partially understood. In chemosensitive leukemias and solid tumors, anticancer drugs have been shown to induce apoptosis. We previously identified activation of the CD95 (APO-1/Fas) receptor/CD95 ligand (CD95/CD95-L) system as a key mechanism for drug-induced apoptosis.

Betulinic acid triggers CD95 (APO-1/Fas)- and p53-independent apoptosis via activation of caspases in neuroectodermal tumors.

Betulinic acid (BA), a melanoma-specific cytotoxic agent, induced apoptosis in neuroectodermal tumors, such as neuroblastoma, medulloblastoma, and Ewing's sarcoma, representing the most common solid tumors of childhood. BA triggered an apoptosis pathway different from the one previously identified for standard chemotherapeutic drugs. BA-induced apoptosis was independent of CD95-ligand/receptor interaction and accumulation of wild-type p53 protein, but it critically depended on activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases).

Cross-resistance of CD95- and drug-induced apoptosis as a consequence of deficient activation of caspases (ICE/Ced-3 proteases).

The cytotoxic effect of anticancer drugs has been shown to involve induction of apoptosis. We report here that tumor cells resistant to CD95 (APO-1/Fas) -mediated apoptosis were cross-resistant to apoptosis-induced by anticancer drugs. Apoptosis induced in tumor cells by cytarabine, doxorubicin, and methotrexate required the activation of ICE/Ced-3 proteases (caspases), similarly to the CD95 system.

The CD95 (APO-1/Fas) system mediates drug-induced apoptosis in neuroblastoma cells.

Anticancer agents have been shown to trigger apoptosis in chemosensitive tumors such as neuroblastomas. We previously identified activation of the CD95 system as one of the key mechanisms for doxorubicin-induced apoptosis in leukemic T cells. Here, we report that therapeutic concentrations of doxorubicin, cisplatinum, and VP-16 led to induction of CD95 receptor and CD95 ligand (CD95-L) that mediated cell death in chemosensitive neuroblastoma cells.

Chronic stomatitis: an early sign of Crohn's disease.

The authors describe an 11-year-old boy who had persistent oral lesions that clinically mimicked first-episode herpetic stomatitis. A biopsy revealed noncaseating sterile granulomas. Investigation of the small and large bowels revealed that the child had Crohn's disease.

Latex-induced asthma in a dental assistant.

In this case report, latex-induced asthma is described in a dental assistant with an associated history of contact dermatitis, contact urticaria, and rhinitis. She switched to vinyl gloves, which eliminated her cutaneous symptoms, but her respiratory symptoms continued. Skin-testing to latex was strongly positive.

Involvement of the CD95 (APO-1/FAS) receptor/ligand system in drug-induced apoptosis in leukemia cells.

Cytotoxic drugs used in chemotherapy of leukemias and solid tumors cause apoptosis in target cells. In lymphoid cells the CD95 (APO-1/Fas)/CD95 ligand (CD95-L) system is a key regulator of apoptosis. Here we describe that doxorbicin induces apoptosis via the CD95/CD95-L system in human leukemia T-cell lines.