Novel mold-resistant building materials impregnated with thermally reduced nano-silver.

In this study, we evaluated the long-term antifungal effectiveness of 3 types of interior building materials (gypsum board [GB], cement board [CB], and softwood plywood [S-PW]) impregnated with thermally reduced silver nanoparticles supported by titanium dioxide (AgNPs/TiO2 ) under 95% relative humidity for 4 weeks. AgNPs/TiO2 was synthesized at 2 thermal reduction temperatures (TRTs, 120 and 200°C) with 2 different AgNP weight percentages (2 and 5 wt%). Four different silver-loading levels (SLLs, 0.025, 0.05, and 0.5 µg/cm2 and the critical concentration required to inhibit fungal growth on agar plates) and 3 fungal species (Aspergillus niger, Penicillium spinulosum, and Stachybotrys chartarum) were used in the experiments. Higher temperature reduced more ionic Ag+ to metallic Ag0 and increased the dispersion of Ag on TiO2 surface. The 200°C thermally reduced AgNPs/TiO2 demonstrated excellent antifungal efficiency: Mold growth was almost completely inhibited for 28 days at the low SLL of 0.5 µg/cm2 . Additionally, AgNPs/TiO2 exhibited higher antifungal activity on GB and CB than on S-PW. The stepwise regression results indicated that the TRT of AgNPs/TiO2 (ß = -0.739 to -0.51), the SLL (ß = -0.477 to -0.269), and the Ag0 level in the AgNPs (ß = -0.379 to -0.136) were the major factors influencing antifungal activity and TRT might be the most significant one.

Identification of a locus for disseminated superficial actinic porokeratosis at chromosome 12q23.2-24.1.

Disseminated superficial actinic porokeratosis is an autosomal dominant cutaneous disorder characterized by many uniformly small, minimal, annular, anhidrotic, and keratotic lesions. The genetic basis for this disease is unknown. Using a genomewide search in a large Chinese family, we identified a locus at chromosome 12q23.2-24. 1 responsible for disseminated superficial actinic porokeratosis. The fine mapping study indicates that the disseminated superficial actinic porokeratosis gene is located within a 9.6 cM region between markers D12S1727 and D12S1605, with a maximum two-point LOD score of 20.53 (theta = 0.00) at D12S78. This is the first locus identified for a genetic disease where the major phenotype is porokeratosis. The study provides a map location for isolation of a gene causing disseminated superficial actinic porokeratosis.

[Molecular clonging of the human dimethyglycine dehydrogenase-like gene (DMGDHL1) from the sarcosinemia critical region at 9q34].

Through the analysis of EST database, we obtained one human EST (GenBank: H28856) which showed significant similarity with the partial coding sequence of rat dimethylglycine dehydrogenase gene. This EST was mapped to 9q34 due to 95.6% identity with one genomic sequence (GenBank: AC002295). A pair of primers (HRP-1/HRP-2) designed on the sequence of the EST were coupled with the primers (lambda gt10-5/lambda gt10-3) on the vector flanking cloning site respectively to amplify the 5' and 3' cDNA beyond the EST. New primers designed based on novel cDNA sequence overlapped with the sequence within EST H28856 were used for amplification with lambda gt10-5 and lambda gt10-3 by the similar way as above untill a complete ORF was obtained. Finally, a 1,970 bp sequence (termed as dimethylglycine dehydrogenase like gene isoform I, DMGDHL1a) containing a 1,428 bp complete coding sequence from the live cDNA library and 1,475 bp sequence (isoform II, termed as DMGDHL1b) containing a 1,296 bp complete coding sequence from the fetas live cDNA library were obtained. Fourteen exons were identified in isoform I and the first nine exons of isoform II which shared with isoform I could be determined too. The last 105 bp cDNA sequence of isoform II could not be found in the public database, indicating a very large intron (> 123 kb) existed between exon 9 and exon 10 of isoform II. DMGDHL1 showed highly homology on both cDNA and amino acid level with rat dimethylglycine dehydrogenase (60% identity in 135 bp and 35% identity in 436 residues respectively). It was reported that human sarcosinemia gene was mapped at 9q34. Therefore it could be a good candidate gene for the sarcosinemia.

Mutations in the gene encoding gap junction protein beta-3 associated with autosomal dominant hearing impairment.

Hearing impairment is the most commonly occurring condition that affects the ability of humans to communicate. More than 50% of the cases of profound early-onset deafness are caused by genetic factors. Over 40 loci for non-syndromic deafness have been genetically mapped, and mutations in several genes have been shown to cause hearing loss. Mutations in the gene encoding connexin 26 (GJB2) cause both autosomal recessive and dominant forms of hearing impairment. To study the possible involvement of other members of the connexin family in hereditary hearing impairment, we cloned the gene (GJB3) encoding human gap junction protein beta-3 using homologous EST searching and nested PCR. GJB3 was mapped to human chromosome 1p33-p35. Mutation analysis revealed that a missense mutation and a nonsense mutation of GJB3 were associated with high-frequency hearing loss in two families. Moreover, expression of Gjb3 was identified in rat inner ear tissue by RT-PCR. These findings suggest that mutations in GJB3 may be responsible for bilateral high-frequency hearing impairment.

Limitations on the parallel guidance of visual search: color x color and orientation x orientation conjunctions.

In visual search for a conjunction it is much more difficult to search for the conjunction of 2 colors or 2 orientations than for Color x Orientation or Color x Shape conjunctions. The result is not limited to particular colors or shapes. Two colors cannot occupy the same spatial location in Color x Color searches. However, Experiments 6 and 7 show that Color x Shape searches remain efficient even if the color and shape are spatially separated. Our guided search model suggests that in searches for Color x Shape, a parallel color module can guide attention toward the correct color, whereas the shape module guides attention toward the correct shape. Together these 2 sources of guidance lead attention to the target. However, if a target is red and green among red-blue and green-blue distractors, it is not possible to guide search independently toward red items and green items or away from all blue items.

Demonstration of intracardiac tumor and its associated hemodynamic derangement by radionuclide angiography.

A case of malignant lymphoma primarily involving the heart is reported for the first time in which the tumor per se and its accompanying hemodynamic abnormalities were demonstrated by radionuclide angiography (RNA). The patient had severe and progressive failure of the right side of the heart of obscure origin. The tumor was pathologically proven to have involvement of the pericardium, right atrium, and right ventricle, causing significant tricuspid and pulmonic obstruction.

A Northern California Oncology Group randomized trial of leucovorin plus 5-fluorouracil versus sequential methotrexate, 5-fluorouracil, and leucovorin in patients with advanced colorectal cancer who failed treatment with 5-fluorouracil or 5-fluorodeoxyuridine alone.

The current study was initiated to confirm preliminary reports that 20% or more of patients with colorectal cancer who fail treatment with 5-fluorouracil (FUra) will respond to treatment with either leucovorin plus FUra or with sequential methotrexate, FUra, leucovorin. One hundred two patients with advanced, measureable colorectal cancer who failed treatment with FUra and/or 5-fluorodeoxyuridine (FUdR) were randomized to treatment with either high-dose leucovorin plus FUra (Arm B) or sequential methotrexate, FUra, leucovorin (Arm C). In this interim report, 92 patients were evaluable for toxicity and 89 patients were evaluable for response. Grade 3 or 4 nonhematologic toxicity which was primarily gastrointestinal was experienced by 25% of patients on both treatment arms during at least 1 treatment cycle. Hematologic toxicity was minimal. Among 43 evaluable patients on Arm B, there were 2 complete responses (5%) and 1 minor response (3%). Among 46 evaluable patients on Arm C, there was 1 complete response (2%), 1 partial response (2%), and 6 minor responses (14%). The median time to treatment failure was 2.2 months on Arm B and 3.5 months on Arm C. The median survival was 8.3 months on Arm B and 8.7 months on Arm C. Colorectal cancers that are resistant to FUra are cross-resistant to both experimental combinations.

Treatment of lymphoblastic lymphoma in adults.

Forty-four adult patients with lymphoblastic lymphoma (LBL) were treated according to one of two protocols. Both included (1) induction with cyclophosphamide, doxorubicin, vincristine, prednisone, and L-asparaginase; (2) CNS prophylaxis; and (3) maintenance therapy with methotrexate (MTX) and 6-mercaptopurine. In the second protocol, CNS prophylaxis began earlier than in the first protocol and included cranial irradiation and intrathecal (IT) MTX rather than simultaneous high-dose systemic and IT MTX. The overall response rate was 100% (95% complete). With a 26-month median follow-up, the 1-and 3-year actuarial freedom from relapse (FFR) for the composite patient group was 70% and 56%, respectively. The incidence of CNS relapse was reduced from 31% in the first protocol to 3% in the second protocol (P = .04, Gehan). Patients can be assigned retrospectively to low (n = 19) and high (n = 25) risk prognostic groups, as indicated by a multivariate analysis of pretreatment prognostic factors. High-risk is defined by Ann Arbor stage IV disease with bone marrow or CNS involvement or initial serum lactate dehydrogenase (LDH) concentration of greater than 300 IU/L (normal, less than 200). FFR of low- and high-risk groups at 5 years are 94% and 19%, respectively (P = .0006). Low-risk patients are highly curable using this approach to adult LBL. More intensive treatment for high-risk patients is warranted.

Phase II study of sequential methotrexate and 5-FU plus mitomycin and leucovorin in patients with disseminated large bowel cancer: a Northern California Oncology Group study.

Sequential methotrexate (MTX) and 5-FU plus leucovorin and mitomycin (MMC) was given to 52 patients with disseminated, measurable colorectal cancer. Complete and partial responses were seen in 19 of 49 (39%) evaluable patients. Nine additional patients achieved a minimal response. Median overall survival was 8.8 months, while that for patients objectively responding was 13.6 months. This study utilized a MTX exposure period of 12 hours prior to 5-FU. In comparison to other trials utilizing sequential MTX and 5-FU, the addition of MMC to the regimen may improve the response rate but increases the incidence of adverse effects, particularly myelosuppression and renal toxicity. This phase II trial suggests that sequential MTX and 5-FU plus leucovorin and MMC is an active combination therapy and warrants further comparative trial in patients with large bowel cancer.