Fractionation of Aspen Wood to Produce Microcrystalline, Microfibrillated and Nanofibrillated Celluloses, Xylan and Ethanollignin.

A new method for extractive-catalytic fractionation of aspen wood to produce microcrystalline (MCC), microfibrillated (MFC), nanofibrilllated (NFC) celluloses, xylan, and ethanollignin is suggested in order to utilize all of the main components of wood biomass. Xylan is obtained with a yield of 10.2 wt.

Microfibrillated Cellulose with a Lower Degree of Polymerization; Synthesis via Sulfuric Acid Hydrolysis under Ultrasonic Treatment.

A new approach is being considered for obtaining microfibrillated cellulose with a low degree of polymerization by sulfuric acid hydrolysis with simultaneous ultrasonic treatment under mild conditions (temperature 25 °C, 80% power control). Samples of initial cellulose, MCC, and MFC were characterized by FTIR, XRF, SEM, DLS, and TGA. It was found that a high yield of MFC (86.

Composition and Structure of Aspen () Hemicelluloses Obtained by Oxidative Delignification.

In this study, hemicelluloses of aspen wood () were obtained by oxidative delignification in an acetic acid-water-hydrogen peroxide medium at temperatures of 70-100 °C and a process time of 1-4 h. The maximum polysaccharide yield of up to 9.68 wt% was reported.

Molecular Characteristics and Antioxidant Activity of Spruce () Hemicelluloses Isolated by Catalytic Oxidative Delignification.

Spruce () wood hemicelluloses have been obtained by the noncatalytic and catalytic oxidative delignification in the acetic acid-water-hydrogen peroxide medium in a processing time of 3-4 h and temperatures of 90-100 °C. In the catalytic process, the HSO, MnSO, TiO, and (NH)MoO catalysts have been used. A polysaccharide yield of up to 11.

[The possibility of prognosis incidence by means of degrees of cancer aggravated family history].

Background: Aim of the study was to estimate the possibility of prognosis incidence by means of degrees of cancer aggravated family history.

Patients And Methods: 1233 families (n = 4689) from the Moscow Cancer Family Registry who answered 5-years later the first questionnaire were divided into 4 groups according to our classification of degrees of cancer aggravated family history: (1) not aggravated, (2) little aggravated, (3) aggravated, (4) syndromes (see detailed description in the text). The methods of genetic epidemiology, epidemiology, statistics were used.

[Sodium nitrite-induced potentiation of spontaneous and 1,2-dimethylhydrazine-induced carcinogenesis in male mice F1 (C57 B1xCBA)].

Chronic sodium nitrite (SN) treatment potentiated spontaneous and 1,2-dimethylhydrazine (DMH)-induced carcinogenesis. Mice injected with SN alone showed a higher incidence of leukemia and lung cancer than in controls. Combined treatment with DMH and SN induced most of benign and malignant tumors (hepatic hemangioendothelioma, hepatocarcinoma, renal adenoma, etc.

[Prospective study of families on a genetic cancer registry].

The Familial Cancer Register, Moscow, established in 1990, has a record of pedigrees of 6,000 cancer patients. The records on the probands and families have been studied since 1995. The paper presents the data of a repeat survey of the families conducted in 1990-1995.

Mechanisms underlying mismatch repair deficiencies in normal cells.

Hereditary nonpolyposis colon cancer (HNPCC) is an autosomal dominantly inherited cancer predisposition which is linked to heterozygous mutations in mismatch repair genes. HNPCC tumour cells, in which the remaining wild-type copy of the mismatch repair gene is inactivated, display instability of microsatellite markers reflecting a defect in mismatch repair. Recently, patients carrying either one of two distinct germline mutations in the MLH1 and PMS2 genes were reported to accumulate somatic mutations of microsatellites in untransformed cells.

CpG dinucleotides in the hMSH2 and hMLH1 genes are hotspots for HNPCC mutations.

Hereditary nonpolyposis colon cancer (HN-PCC) is an autosomally inherited predisposition to cancer that has recently been linked to defects in the human mismatch repair genes hMSH2 and hMLH1. The identification of the causative mutations in HNPCC families is desirable, since it confirms the diagnosis and allows the carrier status of unaffected relatives at risk to be determined. We report six different new mutations identified in the hMSH2 and hMLH1 genes of Russian and Moldavian HNPCC families.

[Congenital absence of a kidney in a patient with the basal cell nevus syndrome].

Basal-cell nevus was diagnosed in a 60-year-old patient who suffered for 20 years from multiple basal-cell carcinomas. Autopsy has revealed congenital absence of the right kidney and ureter after his death at the age of 61.

[The association of ovarian cancer with various genetic markers].

The distribution of blood groups AB0, Rh, P1, MN and Haptoglobins among ovarian cancer patients was studied. Significant associations between ovarian cancer and B(III) and MN blood groups as well as the 2-1 variant of haptoglobin were revealed. These data should be kept in mind when forming the high risk groups among population, in relation to ovarian cancer.

[Detection of basal-cell nevus syndrome in patients with multiple skin basiliomas].

Medico-genetic examinations of 122 patients with multiple and/or early-onset basalioma revealed 5 cases of basal cell nevus syndrome. Clinical data on 5 probands and 3 first-degree relatives with the syndrome are presented.

[Assessment of the risk of developing ovarian cancer based on individual and family anamnestic data].

A study of individual and family histories of 200 ovarian cancer patients and 200 healthy controls was concerned with evaluation of 274 factors of risk. It yielded 36 most informative ones. An 80% credibility of screening results was demonstrated when a combination of characteristics was used.

[Genetic epidemiology study of ovarian cancer. I. A comparison of familial and population frequencies].

The frequency of several kinds of cancer among relatives of 200 patients with ovarian cancer was analysed. The annual population incidence was used as a control. Nonrandom familial clustering of ovarian cancer (p less than 0.

An ovarian cancer family: clinical and cytogenetic data.

A family with five ovarian neoplasms in three subsequent generations was studied. Four women had ovarian cancer at age 38, 40, 47, and 53, and one had cystoma ovari at 24. There were other neoplasms and preneoplastic lesions in this family.

[Familial ovarian cancer].

Two families with high incidence of ovarian cancer among the 1st and 2nd degree relatives are described. These were four sisters suffering it in one family (K). In the other family (L) but the proband her mother and two mother's sisters had ovarian cancer.