Expectancy, homework compliance, and initial change in cognitive-behavioral therapy for anxiety.

Belief in one's ability to change is an important cognitive variable related to treatment gains. This study investigated pretreatment expectancy for anxiety change and early homework compliance in relation to initial and total cognitive change in group cognitive-behavioral therapy (CBT) for anxiety. Participants, who met diagnostic criteria for at least 1 anxiety disorder, completed 10 sessions of group CBT. Early homework compliance mediated the relationship between expectancy for anxiety change at baseline and initial change in CBT. In addition, initial cognitive symptom improvement mediated the relationship between homework compliance and posttreatment outcome. These results suggest that expectancy for change is an important cognitive variable that may provide the initial impetus and subsequent momentum for therapeutic involvement and gains. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A 21-mW 8-b 125-MSample/s ADC in 0.09-mm/sup 2/ 0.13-/spl mu/m CMOS

This paper presents an 8-b two-step subranging analog-to-digital (ADC) using interpolation, averaging, offset compensation, and pipelining techniques to accomplish an effective number of bits of 7.6 b at 125 MSample/s. The 0.13-/spl mu/m CMOS ADC occupies 0.09 mm/sup 2/ and consumes 21 mW.     

G-CSF (filgrastim)-stimulated whole blood kept unprocessed at 4 degrees C does support a BEAM-like regimen in bad-risk lymphoma

In most invasive cervical carcinomas, high-risk human papillomavirus (HPV) DNA is integrated into the host genome, while in pre-invasive cervical lesions the viral genome is typically maintained exclusively as an episome. In contrast, integration of low-risk HPV DNA is rare, as is the association of low-risk HPVs with carcinomas. High-risk HPV integration is associated with a selective growth advantage of affected cells, and hence, integration is likely to be an important genetic alteration contributing to cervical tumor progression. Expression of high-risk, but not low-risk, HPV E6 or E7 proteins disrupts the p53-dependent G1 arrest that cells normally display in response to DNA damage. Absence of this cell cycle checkpoint may predispose cells containing high-risk HPVs to genetic instability and to the accumulation of the genetic alterations that appear to be required for HPV-associated cervical tumor progression. We hypothesized that integration of high-risk HPV DNA into the host cell genome may be facilitated by E6- and/or E7-mediated disruption of the normal DNA damage response pathway. To test this hypothesis, we assessed the integration frequency of a reporter plasmid (pHyGal) in RKO cells expressing individual E6 or E7 genes of either high-risk (HPV16) or low-risk (HPV6, HPV11) type viruses. Cells expressing HPV16 E6 or HPV16 E7 exhibited a significantly increased frequency of pHyGal integration in comparison to RKO control cells or cells expressing low-risk HPV E6 or E7. Thus, expression of high-risk, but not low-risk, E6 and E7 proteins increases the frequency of foreign DNA integration into the host genome. These findings suggest that at least some of the difference in oncogenic potential observed between high-risk and low-risk HPV types may be determined by the increased ability of high-risk HPVs to integrate into host DNA.     

An electroencephalographic study of 4-aminopyridine

The electroencephalographic (EEG) effects of 4-aminopyridine (4-AP) given intravenously in therapeutic doses were studied in four conscious human volunteers. 4-AP (0.2 mg/kg) caused an increase of the occipital alpha peak frequency of 0.4 to 1.0 Hz. In the dose range of 0.2 to 0.3 mg/kg there was neither evidence for epileptic activity in the EEG nor were any clinical side effects observed. This dose of 4-AP was also found to antagonize diazepam-induced sleep in four volunteers. In addition 4-AP (0.3 mg/kg) hastened the recovery by a factor of 4 in four patients having endoscopic procedures under diazepam-nitrous oxide anesthesia.     

Identification of the persistently bound form of the carcinogen N-acetyl-2-aminofluorene to rat liver DNA in vivo

In this article the structural analysis of the persistently bound form of the carcinogen N-acetyl-2-aminofluorene (AAF) to rat liver DNA in vivo is described. This compound appears to result from the formation of a covalent bond between carbon-3 of the aromatic ring and the amino group of guanine. Experimental evidence from three different approaches had led to the identification of the structure of the persistently DNA-bound AAF moiety. First, [3-3H, 9-14C]N-acetoxy-AAF was reacted with DNA in vitro. As reported previously, a minor product was isolated from enzymatic digests of the reacted DNA, which had chemical and chromatographic properties identical to those of the persistent--AAF moiety in DNA in vivo. The ratio 3H/14C of this product had diminished to the same extent as 3-CH3S-AAF resulting from the reaction of methionine with [o-3H, 9-14C]N-acetoxy-AAF. Secondly, reaction of [9-14C]N-acetoxy-AAF with DNA, which was tritiated in the C-8 positions of the purines, did not result in removal of tritium in the persistent fraction obtained after acid hydrolysis, thus excluding substitution at C-8 and N-7 of guanine. Finally , by reacting N-OSO3-K-AAF with deoxyguanosine in dimethylsulfoxide-triethylamine, a compound could be isolated, which was identified as 3-(deoxyguanosin-N2-yl)-AAF based on its NMR spectrum and on the mass spectrum of the corresponding guanine derivative obtained after removing deoxyribose by acid hydrolysis. This compound appeared to be identical with the persistently bound form present in DNA hydrolysates from rat liver after injection of [2'-3H]N-hydroxy-AAF.     

Frequency of homozygous deletion at p16/CDKN2 in primary human tumours

BACKGROUND: Carcinoma of the breast is characterized by a variable course with prognosis dependent on disease stage at presentation. Paradoxically, some patients with early malignancy demonstrate disease progression within a short time. The role of tumor markers in the management of carcinoma of the breast is controversial. While CA15-3 is the most widely used tumor marker in carcinoma of the breast, its role in the management of patients with early disease is controversial. STUDY DESIGN: Since 1986, all patients presenting to our unit with carcinoma of the breast have had serial CA15-3 levels measured. This study evaluates the role of serial CA15-3 levels in the management of a consecutive series of 168 patients with Stage I disease at presentation. RESULTS: The mean preoperative CA15-3 levels at presentation were significantly elevated in patients with Stage I disease compared with patients with benign disease. Sixteen patients had either locoregional (five patients) or metastatic recurrence (11 patients). CA15-3 levels were not elevated in patients with locoregional disease and were significantly elevated in patients with bony metastases and gave a mean lead time of 6.3 months over bone scintigraphy. CONCLUSIONS: Serial CA15-3 measurements are an efficient and cost-effective method of monitoring disease progression and have advantages over conventional investigations in patients with early carcinoma of the breast.     

Comparison of oncogene mutation detection and telomerase activity for the molecular staging of non-small cell lung cancer

Novel oncogene mutation detection techniques have demonstrated that standard histopathological examination may fail to detect clinically significant metastatic cancer cells. Recently, telomerase activity has been detected in most immortal cell lines and human tumors, potentially providing a novel diagnostic marker. We compared standard histopathological examination with the telomeric repeat amplification protocol assay and either a p53 plaque hybridization or a K-ras mutation ligation assay in the lymph nodes of 12 patents with surgically resectable non-small cell lung cancer. Telomerase activity was detected in 10 of 10 (100%) evaluable tumors. Eight of 9 (89%) histopathologically positive lymph nodes were telomerase positive, and 26 of 48 (54%) histopathologically negative lymph nodes were telomerase positive. In comparison, oligonucleotide plaque hybridization detected metastases in all 3 histopathologically positive nodes and in 3 of 27 histopathologically negative nodes. Similarly, the K-ras mutation ligation assay detected metastases in all 6 histopathologically positive lymph nodes examined and in 1 of 21 histopathologically negative lymph nodes. Thus, most of the "positive" nodes by telomerase assay did not harbor occult neoplastic cells that shared the same genetic alteration as the primary tumor. The high rate of false positives associated with the telomeric repeat amplification protocol assay limits its role in staging lymph nodes in patients with non-small cell lung cancer.