Zapiski i dnevnik

Half-title: Moi︢a��� povest'o samom sebi︢e︣ i o tom "Chemu svidietel' v zhizni byl."

India, 1804 (Sheet 5 of 6) (Raster Image)

This layer is a georeferenced raster image of the historic paper map entitled: To Mark Wood Esq., M.P. colonel of the Army in India, late Chief Engineer and Surveyor General, Bengal, this map of India, compiled from various interesting and valuable materials, is inscribed in grateful testimony of his liberal communications, by ... A. Arrowsmith ; George Allen sculp. It was published by A. Arrowsmith in 1804. Scale [ca. 1:1,800,000]. This layer is image 5 of 6 total images of the six sheet source map, representing the central east portion of the map. Covers primarily India and adjacent portions of Asia.The image inside the map neatline is georeferenced to the surface of the earth and fit to the Asia North Lambert Conformal Conic coordinate system. All map collar and inset information is also available as part of the raster image, including any inset maps, profiles, statistical tables, directories, text, illustrations, index maps, legends, or other information associated with the principal map. This map shows features such as drainage, cities and other human settlements, roads, territorial boundaries, shoreline features, and more. Relief shown by hachures. Includes also notes on the navigability of rivers.This layer is part of a selection of digitally scanned and georeferenced historic maps from the Harvard Map Collection. These maps typically portray both natural and manmade features. The selection represents a range of originators, ground condition dates, scales, and map purposes.

Janāb-i Ba-davlatnī hikāyātlārī : manuscript, 1904 or 5

An eyewitness account of Yaqub Beg's rule in parts of Xinjiang.

Effects of 2 or 5 consecutive exercise days on adipocyte area and lipid parameters in Wistar rats

Background: Exercise has been prescribed in the treatment and control of dyslipidemias and cholesterolemia, however, lipid responses to different training frequencies in hypercholesterolemic men have been inconsistent. We sought to verify if different frequencies of continuous moderate exercise (2 or 5 days/week, swimming) can, after 8 weeks, promote adaptations in adipocyte area and lipid parameters, as well as body weight and relative weight of tissues in normo and hypercholesterolemic adult male rats.Methods: Normal cholesterol chow diet or cholesterol-rich diet (1% cholesterol plus 0.25% cholic acid) were freely given during 8 weeks to the rats divided in 6 experimentals groups: sedentary normal cholesterol chow diet (C); sedentary cholesterol-rich diet (H); 5x per week continuous training normal cholesterol chow diet (TC5) and cholesterol-rich diet (TH5); 2x per week continuos traning normal cholesterol chow diet (TC2) and cholesterol-rich diet (TH2).Results: No changes were observed in lipid profile in normal cholesterol chow diet, but both 2 a 5 days/week exercise improved this profile in cholesterol-rich diet. Body weight gain was lower in exercised rats. Decrease in retroperitoneal and epididymal relative weights as well as reductions in adipocyte areas under all diets types were observed only in 5 days/week, while 2 days/week showed improvements mainly in cholesterol-rich diet rats.Conclusion: Our results confirm the importance of exercise protocols to control dyslipidemias and obesity in rats. The effects of 5 days/week exercise were more pronounced compared with those of 2 consecutive days/week training.

Effect of deletion of 5'HS3 or 5'HS2 of the human beta-globin locus control region on the developmental regulation of globin gene expression in beta-globin locus yeast artificial chromosome transgenic mice.

To analyze the function of the 5' DNase I hypersensitive sites (HSs) of the locus control region (LCR) on beta-like globin gene expression, a 2.3-kb deletion of 5'HS3 or a 1.9-kb deletion of 5'HS2 was recombined into a beta-globin locus yeast artificial chromosome, and transgenic mice were produced. Deletion of 5'HS3 resulted in a significant decrease of epsilon-globin gene expression and an increase of gamma-globin gene expression in embryonic cells. Deletion of 5'HS2 resulted in only a small decrease in expression of epsilon-, gamma-, and beta-globin mRNA at all stages of development. Neither deletion affected the temporal pattern of globin gene switching. These results suggest that the LCR contains functionally redundant elements and that LCR complex formation does not require the presence of all DNase I hypersensitive sites. The phenotype of the 5'HS3 deletion suggests that individual HSs may influence the interaction of the LCR with specific globin gene promoters during the course of ontogeny.

Salaries & grants voted, 1804 October 5

One folio-sized leaf containing a handwritten copy of certain votes of the Harvard Corporation on October 5, 1804 related to salaries, grants, and appointments.

Ḥāshiyat malik al-ʻulamāʼ Mawlānā ʻAbd al-ʻAlī ʻalá ḍābiṭat Tahdhīb al-manṭiq : manuscript, 1854 or 5

Written in one column, 9 lines per page, in black and red.

Hādhā Arba��ūn ḥadīthan : manuscript, 1824 or 5

According to the colophon (f. 117v), copy completed in the hand of ʻAbd al-Razzāq ibn Muḥammad Ḥusayn al-Yazdī in 1240 AH [December 1824-5 AD].

Kitāb Shurūṭ al-imāmah / lil-Shaykh al-Imām Abū al-ʻAbbās A���mad ibn Ḥamzah al-Ramlī al-Anṣārī al-Shāfiʻī : manuscript, undated

Written in several hands, in one column, 23-24 lines per page, in black rubricated in red.

Lady Hewley's charities : observations on the case of the attorney-general v. Shore and others.

"From the Law Magazine, no. 32."

Authentic report of the discussion on the Unitarian controversy : between the Rev. John Scott Porter and the Rev. Daniel Bagot : held on April 14, 1834, and three following days, in the Meeting House of the First Presbyterian Congregation, Belfast.

Mode of access: Internet.

Chromosome damage induced by 5-azacytidine under the influence of caffeine or cytosine arabinoside in CHO-K1 (wild-type) and XRS-5 (mutant) cell lines

5-azacytidine (5-azaC) treatment combined with cytosine arabinoside (ara-C) or caffeine were performed in vitro in Chinese hamster cells, CHO-K1 (wild-type) and xrs-5 (mutant) cell lines, in order to compare the cell response to the induction of chromosomal aberrations. Exponentially growing cells were treated with 5-azaC (4-16 uM) for 1 h, the cells were washed and incubated for 7 h, and 500 uM caffeine or 5 uM ara-C were added to the cultures for the last 2 h. In both cell lines, 5-azaC induced a significantly increase (P<0.01) in the frequencies of aberrations; in the combined treatments (5-azaC + Ara-C), a significant reduction (P<0.05) was observed for the aberrations which were randomly distributed. Caffeine had no influence at the same conditions. 5-azaC induced-DNA lesions were probably processed at S/G2 phase in a common pathway in both cell lines, but alternatively, 5-azaC may cause xrs-5 cells to revert to the wild-type.

Immunologic characteristics of immunogenic variants generated by {\it in vitro\/} treatment of a methylcholanthrene-induced murine fibrosarcoma MCA-F with 1 methyl-3-nitro-1-nitrosoguanidine, 5 -aza-2$\sp\prime$-deoxycytidine, or ultraviolet radiation

This study addresses the questions of whether the frequency of generation and in vivo cross-reactivity of highly immunogenic tumor clones induced in a single parental murine fibrosarcoma cell line MCA-F is more closely related to the agent used to induce the Imm$\sp{+}$ clone or whether these characteristics are independent of the agents used. These questions were addressed by treating the parental tumor cell line MCA-F with UV-B radiation (UV-B), 1-methyl-3-nitro-1-nitrosoguanidine (MNNG), or 5-aza-2$\sp\prime$-deoxycytidine (5-azaCdR). The frequency of Imm$\sp{+}$ variant generation was similarly high for the three different agents, suggesting that the frequency of Imm$\sp{+}$ generation was related more closely to the cell line than to the inducing agent used. Cross-reactivity was tested with two Imm$\sp{+}$ clones from each treatment group in a modified immunoprotection assay that selectively engendered antivariant, but not antiparental immunity. Under these conditions each clone, except one, immunized against itself. The MNNG-induced clones engendered stronger antivariant immunity but a weaker variant cross-reactive immunity could also be detected.^ This study also characterized the lymphocyte populations responsible for antivariant and antiparental immunity in vivo. Using the local adoptive transfer assay (LATA) and antibody plus complement depletion of T-cell subsets, we showed that immunity induced by the Imm$\sp{+}$ variants against the parent MCA-F was transferred by the Thy1.2$\sp{+}$, L3T4a$\sp{+}$, Lyt2.1$\sp{-}$ (CD4$\sp{+}$) population, without an apparent contribution by Thy1.2$\sp{+}$, L3T4a$\sp{-}$, Lyt2.1$\sp{+}$ (CD8$\sp{+}$) cells. A role for Lyt2.1$\sp{+}$T lymphocytes in antivariant, but not antiparent immunity was supported by the results of LATA and CTL assays. Immunization with low numbers of viable Imm$\sp{+}$ cells, or with high numbers of non viable Imm$\sp{+}$ cells engendered only antivariant immunity without parental cross-protection. The associative recognition of parental antigens and variant neoantigens resulting in strong antiparent immunity was investigated using somatic cells hybrids of Imm$\sp{+}$ variants of MCA-F and an antigenically distinct tumor MCA-D. An unexpected result of these latter experiments was the expression of a unique tumor-specific antigen by the hybrid cells. These studies demonstrate that the parental tumor-specific antigen and the variant neoantigen must be coexpressed on the cell surface to engender parental cross-protective immunity. (Abstract shortened with permission of author.) ^

Reversal of acute coagulopathy during hypotensive resuscitation using small-volume 7.5% NaCl adenocaine and Mg2+ in the rat model of severe hemorrhagic shock

OBJECTIVE: : Acute traumatic coagulopathy occurs early in hemorrhagic trauma and is a major contributor to mortality and morbidity. Our aim was to examine the effect of small-volume 7.5% NaCl adenocaine (adenosine and lidocaine, adenocaine) and Mg on hypotensive resuscitation and coagulopathy in the rat model of severe hemorrhagic shock. DESIGN: : Prospective randomized laboratory investigation. SUBJECTS: : A total of 68 male Sprague Dawley Rats. INTERVENTION: : Post-hemorrhagic shock treatment for acute traumatic coagulopathy. MEASUREMENTS AND METHODS: : Nonheparinized male Sprague-Dawley rats (300-450 g, n = 68) were randomly assigned to either: 1) untreated; 2) 7.5% NaCl; 3) 7.5% NaCl adenocaine; 4) 7.5% NaCl Mg; or 5) 7.5% NaCl adenocaine/Mg. Hemorrhagic shock was induced by phlebotomy to mean arterial pressure of 35-40 mm Hg for 20 mins (~40% blood loss), and animals were left in shock for 60 mins. Bolus (0.3 mL) was injected into the femoral vein and hemodynamics monitored. Blood was collected in Na citrate (3.2%) tubes, centrifuged, and the plasma snap frozen in liquid N2 and stored at -80°C. Coagulation was assessed using activated partial thromboplastin times and prothrombin times. RESULTS: : Small-volume 7.5% NaCl adenocaine and 7.5% NaCl adenocaine/Mg were the only two groups that gradually increased mean arterial pressure 1.6-fold from 38-39 mm Hg to 52 and 64 mm Hg, respectively, at 60 mins (p < .05). Baseline plasma activated partial thromboplastin time was 17 ± 0.5 secs and increased to 63 ± 21 secs after bleeding time, and 217 ± 32 secs after 60-min shock. At 60-min resuscitation, activated partial thromboplastin time values for untreated, 7.5% NaCl, 7.5% NaCl/Mg, and 7.5% NaCl adenocaine rats were 269 ± 31 secs, 262 ± 38 secs, 150 ± 43 secs, and 244 ± 38 secs, respectively. In contrast, activated partial thromboplastin time for 7.5% NaCl adenocaine/Mg was 24 ± 2 secs (p < .05). Baseline prothrombin time was 28 ± 0.8 secs (n = 8) and followed a similar pattern of correction. CONCLUSIONS: : Plasma activated partial thromboplastin time and prothrombin time increased over 10-fold during the bleed and shock periods prior to resuscitation, and a small-volume (~1 mL/kg) IV bolus of 7.5% NaCl AL/Mg was the only treatment group that raised mean arterial pressure into the permissive range and returned activated partial thromboplastin time and prothrombin time clotting times to baseline at 60 mins.