Online therapy: review of relevant definitions, debates, and current empirical support

The current article reviews the most recent literature addressing the definitions, ethical considerations, and potential strengths and limitations of online therapy. In addition, a framework is provided for how to conceptualize and categorize different aspects of online therapy for research purposes. Relevant studies of both online and face-to-face therapy as well as suggestions for future research are outlined.     

En bloc vs transhiatal esophagectomy for stage T3 N1 adenocarcinoma of the distal esophagus

HYPOTHESIS: En bloc esophagectomy (EBE) provides improved survival over transhiatal esophagectomy (THE) in patients with similarly sized transmural tumors (T3) and lymph node metastases (N1). DESIGN: A retrospective case-control study of 2 methods of esophageal resection for cancer. SETTING: University hospital (tertiary referral center for esophageal disease). PATIENTS: There were 49 patients (27 who underwent EBE and 22 who underwent THE) with similar T3 N1 disease and the following matched criteria: tumors of similar size and location, more than 20 lymph nodes in the surgical specimen, R0 resection, no previous chemotherapy or radiation therapy, and follow-up until death or for a minimum of 5 years.Main Outcome Measure Survival adjusted for differences in demographic and patient characteristics. RESULTS: The number of nodes harvested was greatest after EBE vs THE (median, 52 vs 29 [range, 21-85 vs 20-60]; P<.001). The median number of involved nodes was similar after EBE vs THE (median, 5 vs 7 [range, 1-19 vs 1-16]). The only 2 independent factors that affected survival in a Cox analysis were the number of involved lymph nodes (P =.01) and the type of resection (P =.03). Patients who underwent EBE had a survival benefit over those who underwent THE (P =.01). The survival benefit of EBE was seen only in patients with fewer than 9 involved lymph nodes (P<.001). CONCLUSION: En bloc esophagectomy confers a better survival than THE in patients with T3 N1 disease and fewer than 9 lymph node metastases.     

Lymphadenectomy prior to rat hind limb allotransplantation prevents graft-versus-host disease in chimeric hosts

In previous rat studies, the use of mixed allogeneic chimerism (MAC) to induce host tolerance to hind limb allografts has resulted in severe graft-versus-host disease (GVHD). The purpose of this study was to determine if immunocompetent cells in bone marrow (BM) and/or lymph nodes (LNs) of transplanted limbs were responsible for inducing GVHD in mixed chimeric hosts. [ACIWistar Furth] chimeric rats received ACI hind limbs that were non-irradiated, irradiated (1050 cGy) or lymphadenectomized. Rejection, GVHD and donor chimerism was assessed. Chimeric hosts rejected none of their limbs. However, hosts of non-irradiated hind limbs succumbed to GVHD 22.4±0.8 days after transplantation. In contrast, chimeras that received irradiated or lymphadenectomized ACI hind limbs showed no clinical or histological signs of GVHD at 5 months. We conclude that mixed chimeric hosts are susceptible to GVHD due to the immunocompetent cell load provided by the LNs, not the BM, of hind limb allografts.Abbreviations BM Bone marrow - CPM Counts per minute - CTA Composite tissue allograft - FACS Fluorescence activated cell sorter - FITC Fluorescent iso-thiocyanate - GVH Graft-versus-host - GVHD Graft-versus-host disease - HVG Host-versus-graft - LN Lymph node - MAC Mixed allogeneic chimerism - MHC Major histocompatibility complex - MLR Mixed lymphocyte reaction - MoAb Monoclonal antibody - PBL Peripheral blood lymphocytes - SEM Standard error of mean - TBI Total body irradiation - TCD T-cell depletion/T-cell depleted - TCR T-cell receptor     

Interaction between adenosine and allergen or compound 48/80 on lung parenchymal strips from actively sensitized Brown Norway rats

We have investigated the effect of mast cell activation induced by immunological and non-immunological stimuli on the sensitivity to adenosine of parenchymal strips prepared from lungs removed from Brown Norway (BN) rats actively sensitized to ovalbumin. Strips responded to ovalbumin with a biphasic contractile response. Responses to adenosine were markedly increased 30 min after ovalbumin. The first phase of the response to ovalbumin was abolished by the 5-hydroxytryptamine (5-HT)2 receptor antagonist, methysergide and unaffected by the cysteinyl leukotriene receptor antagonist, iralukast. The second phase was abolished by iralukast and unaffected by methysergide. The response to adenosine was markedly reduced by methysergide but not significantly altered by iralukast. Compound 48/80 (condensation product of N-methyl-p-methoxyphenylethylamine with formaldehyde) induced methysergide-sensitive contractions of the parenchymal strip and potentiated adenosine; the augmented response to adenosine was blocked by methysergide. Thus, activation of mast cells in the lung by either immunological or non-immunological stimuli results in augmentation of the mast cell-mediated contractile response to adenosine.     

Deformable image registration for the use of magnetic resonance spectroscopy in prostate treatment planning

PURPOSE: There is now convincing evidence that prostate cancer cells lack the ability to produce and accumulate citrate. Using magnetic resonance spectroscopy imaging (MRSI), regions of absent or low citrate concentration in the prostate can be visualized at a resolution of a few mm. This new advancement provides not only a tool for early diagnosis and screening but also the opportunity for preferential targeting of radiation to regions of high tumor burden in the prostate. The differences in the shape and location of the prostate between MRSI imaging and treatment have been the major obstacle in integrating MRSI in radiation therapy treatment planning. The purpose of this study is to develop a reliable method for deforming the prostate and surrounding regions from the geometry of MRSI imaging to the geometry of treatment planning, so that the regions of high tumor burden identified by the MRSI study can be faithfully transferred to the images used for treatment planning. METHODS AND MATERIALS: Magnetic resonance spectroscopy imaging studies have been performed on 2 prostate cancer patients using a commercial MRSI system with an endorectal coil and coupling balloon. At the end of each study, we also acquired the MRI of the pelvic region at both the deformed state where the prostate is distorted by the endorectal balloon and the resting state with the endorectal balloon deflated and removed. The task is to find a three-dimensional matrix of transformation vectors for all volume elements that links the two image sets. We have implemented an optimization method to iteratively optimize the transformation vectors using a Newton-Ralphson algorithm. The objective function is based on the mutual information. The distorted images using the transformation vectors are compared with the images acquired at the resting conditions. RESULTS AND DISCUSSION: The algorithm is capable of performing the registration automatically without the need for intervention. It does not require manual contouring of the organs. By applying the algorithm to multiple image sets of different patients, we found a good agreement between the images transformed from those acquired at the deformed state and those acquired at resting conditions. The computation time required for achieving the registration is in the range of a half-hour (for image size: 256 pixels x 256 pixels x 25 slices). However, the space of registration can be restricted to speed up the process. CONCLUSION: In this article, we described a three-dimensional deformable image registration method to automatically transform images from the deformed imaging state to resting state. Our examples show that this method is feasible and useful to the treatment planning system.     

Upregulation of group 1 CD1 antigen presenting molecules in guinea pigs with experimental autoimmune encephalomyelitis: an immunohistochemical study

In humans, group 1 CD1 glycoproteins present foreign and self lipid and glycolipid antigens to T-cells. Homologues of these molecules are not found in mice or rats but are present in guinea pigs (GPs). We examined CD1 and MHC class II expression in the central nervous system (CNS) of GPs sensitized for experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. In normal GPs and the uninflamed CNS, low-level MHC class II (MHC II) immunoreactivity occurred on vascular elements, meningeal macrophages and parenchymal microglial cells, whereas immunoreactivity for CD1 was absent. In the inflamed CNS, the majority of infiltrating cells were MHC II+ and microglia showed increased expression. CD1 immunoreactivity was detected on astrocytes and subsets of inflammatory cells Including B cells and macrophages. Minimal CD1 and MHC II co-expression was noted on inflammatory cells or glia. We conclude that group 1 CD1 molecules are strongly upregulated in the inflamed CNS on subsets of cells distinct from the majority of MHC II bearing cells. The expression of CD1 proteins in such lesions broadens the potential repertoire of antigens recognized at these sites and highlights the value of the GP as a model for studies of the relevance of CD1 molecules in host defense and autoimmune diseases.     

Congenital hypopituitarism as a cause of undetectable estriol levels in the maternal triple-marker screen

We are reporting a child with congenital panhypopituitarism, in whom deficient fetal steroidogenesis was suspected prenatally because of undetectable estriol levels measured in the maternal triple-marker screen. No fetal abnormalities were detected by ultrasonography. Amniocentesis demonstrated a normal 46,XX karyotype. Measurement of maternal urinary steroids failed to show elevation in the excretion of the major precursor for estriol, 16 alpha-hydroxydehydroepiandrosterone, indicating that the fetus did not have steroid sulfatase deficiency (placental sulfatase deficiency), the most common genetic cause of extremely low estriol. The steroid analysis excluded other rare single gene defects, including aromatase deficiency and 17 alpha-hydroxylase deficiency. We therefore suspected that the cause of low estriol in this fetus was adrenal insufficiency. Postnatal evaluation was consistent with panhypopituitarism, characterized by deficiency of all anterior pituitary hormones. Because this screen is now offered to more than half the pregnant women in the United States, reports of low estriol levels have become increasingly common. Therefore, it is essential that physicians be familiar with the various etiologies, perform the appropriate antenatal evaluation to determine the specific cause, and closely monitor both mother and child ante- and postnatally.     

The diagnosis of congenital adrenal hyperplasia in the newborn by gas chromatography/mass spectrometry analysis of random urine specimens

Definitive neonatal diagnosis of congenital adrenal hyperplasia (CAH) is frequently complicated by normal 17-hydroxyprogesterone levels in 21-hydroxylase-deficient patients, residual maternal steroids, and other interfering substances in neonatal blood. In an effort to improve the diagnosis, we developed a gas chromatography/mass spectrometry method for simultaneous measurement of 15 urinary steroid metabolites as early as the first day of life. Furthermore, we developed 11 precursor/product ratios that diagnose and clearly differentiate the four enzymatic deficiencies that cause CAH. Random urine samples from 31 neonatal 21-hydroxylase-deficient patients and 59 age-matched normal newborns were used in the development. Additionally, samples from two 11 beta-hydroxylase-deficient patients and one patient each for 17 alpha-hydroxylase and 3 beta-hydroxysteroid dehydrogenase deficiencies were used. The throughput for one bench-top gas chromatography/mass spectrometry instrument is 20 samples per day. Thus, this method affords an accurate, rapid, noninvasive means for the differential diagnosis of CAH in the newborn period without the need for invasive testing and ACTH stimulation.     

Women and small cell lung cancer: social characteristics, medical history, management and survival: a retrospective study of all the male and female cases diagnosed in Bas-Rhin (Eastern France) between 1981 and 1994

The literature make it clear that lung cancer in women differs from that in men in several specific aspects. We conducted a retrospective study of the 967 consecutive recorded patients (696 men and 91 women after exclusions) diagnosed with small cell lung cancers (SCLC) between 1981 and 1994 in the Bas-Rhin population-based cancer registry to determine if such particularities could be observed in SCLC. Data included demographic and social characteristics, medical and smoking history, management (diagnosis and treatment), hospitalisation and survival. The end point for survival was 31 December 1998. Women were more frequently single, divorced, or widowed (P=0.007) and lived more often in urban areas (places with more than 10,000 inhabitants) (P=0.017). They differed significantly from men in their tobacco exposure (P=0.0001) and non-smoking rates (P=0.0003) but not in clinical presentation, except for more frequently elevated LDH levels (P=0.02). Bone marrow biopsies were more often performed in men (P=0.004), but management was otherwise comparable. The mean number of hospitalisations (for any reason) was comparable in both sexes but women tended to remain hospitalised longer (P=0.057). Overall survival did not differ, but women older than 70 years died sooner than their male counterparts (P=0.026). Our study confirms that some of gender differences reported in the lung cancer literature exist in SCLC. Sex-related differences in LDH levels have not previously been reported, to our knowledge. North American and European data concerning survival among women and men are discordant. Whether these gender differences are related to a real difference between the sexes or simply to differential exposure to carcinogens remains to be determined.