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In this paper in all 6 fungi three of which viz.Helminthosporium dorycarpum, Tetrasporium asterinearum andDiploida sp. growing as hyperparasites onMeliola sp.,Meliola aethiops var.cassiae var. nov. andPhyllachora sacchari spontanei respectively are recorded and described.

In this paper seven new and economically important hosts to the genusLeptosphaerulina are reported and the morphology of the fungi described.Leptosphaerulina ricini onRicinus communis, L. brassicae onBrassica nigra, B. oleracea var.capitata andB. oleracea var.botrytis; Leptosphaerulina australisMcAlp. onCyamopsis tetragonoloba, Phaseolus sp., andLeptosphaerulina oryzae comb. nov. onOryza sativa.

During the crop season of 1954, a downy mildew inciting spotting of leaves and grains of Sorghum vulgare was collected at the Agricul? ture Farm, Oosmania University, Hyderabad. The disease was unlike that of the downy mildew Sclerospora sorghi Weston & Uppal, which causes shredding of leaves, developing numerous oospores, and is wide? spread in the sorghum-growing areas of the states of Mysore, Bombay and Hyderabad. A detailed morphological study of the disease-inciting organism revealed that the fungus was an undescribed member of the Peronosporales, related in a general way to Peronospora and Sclerospora, but distinct from all the members so far described.

Desynapsis leading to total sterility was observed in one plant of Job's tears, Coix lacrymajobi. L., during summer months, while the other neighbouring plants were quite normal. Pachytene chromosome pairing in the desynaptic was apparently normal but a diakinesis and metaphase I several univalents were found. Perennial suckers of this plant in the rainy season showed regular meiosis and good fertility. It is probable that desynapsis was caused by an interaction of genotype and environment, in which the desynaptic gene became activated by the rapid increase in summer temperatures whilst its effect on chromosome synapsis was completely lost in the cooler periods.

Two cases of reversion to diploidy were observed in autotetraploid Job's tears (Coix lacryma-jobi L. 4n = 40) out of a total of 1,112 plants examined over a period of 7 years. One of these was a trisomie (2n = 21) and the other a disomic (2n = 20), derived from apomictic development ofn+1 andn maternal gametes of the tetraploid, respectively. In some respects both these derivatives differed from the original diploid that gave rise to the tetraploid through colchicine treatment. The potentialities of such reversions in the evolution of new diploid races are discussed.

The yellow striping in Job's tears showed nonchromosomal maternal inheritance of the trait producing green, yellow lethal and striped seedlings in the offspring in widely different ratios whenever the striped plant was used as female parent. Plastids in yellow regions of the striped plant were of various sizes and colours ranging from normal to minute size and light yellow or pale green to transparent ones. They were even absent in some cells. The plastids in the leaves of the yellow lethals were usually pale green. While the histological studies indicate the probability that the genetic determinants affecting plastids were in the cytoplasm, the possibility that all the abnormal plastid types could be different expressions of the same original mutation that occurred in the plastids, together with the extensive data on the breeding behaviour of the striped plant, is strongly in favour of the concepts of plastid mutation and autonomy.

The purpose of this study was to demonstrate that in vitro cell culture systems could serve a useful purpose in providing some guidelines in formulating drug schedules for combination cancer chemotherapy in the clinic. Using monolayer cultures of Chinese hamster ovary cells as the test system, we screened the combinations of 1-beta-D-arabinofuranosylcytosine (ara-C) + adriamycin, ara-C + 3,6 - BIS(5 - CHloro - 2 - piperidinyl) - 2,5 - piperazinedione, melphalan + 5-fluorouracil, and melphalan + ara-C as to the effect of drug sequence on the plating efficiency of these cells. Schedule-dependent therapeutic synergism was observed only when ara-C treatment was followed by either adriamycin or 3,6-bis(5-chloro-2-piperidinyl)2,5-piperazinedione but not vice versa. No synergistic effects were observed in the combination of melphalan with 5-fluorouracil or ara-C. The basis for this synergism appeared to be that ara-C was primarily acting as a synchronizing agent to set up the cells in S phase so that subsequent treatment with an S-phase-specific drug, such as adriamycin or 3,6-bis(5-chloro-2-piperidinyl)-2,5-piperazinedione, would produce the maximum cell kill. On the other hand, the lack of synergism in the combinations of melphalan with 5-fluorouracil or ara-C was due to the lack of S-phase specificity for melphalan. On the basis of these data, we postulate that schedule-dependent synergism could be expected if the first agent renders the cells more sensitive (for example, by selectively blocking cells in one of the phases of the cell cycle) to the action of the second drug.

The short- and long-term effects of adriamycin treatment on the cell cycle kinetics and chromosome structure of Chinese hamster ovary cells were investigated. Adriamycin treatment, either pulse or continuous, did not delay the progression of G1 cells into S phase but did prolong the duration of S and G2 phases. This effect was dose dependent, and the prolongation of G2 period was greater than that of S. The frequency of chromosomal aberrations induced by adriamycin was studied in the mitotic as well as in the prematurely condensed chromosomes (PCC) of the treated cells. The types of aberrations observed were chromosome stickiness, chromatid exchanges, breaks, and gaps. The frequency of aberrations continued to increase as cells progressed to mitosis even after the removal of drug from the medium. At prolonged intervals (24 to 72 hr) after a brief or extended treatment, the labeling indices of the treated populations decreased, indicating an eventual block in the cell cycle progression. Visualization of chromosomes of these blocked interphase cells by the PCC method revealed that normal G2 PCC were totally absent. We observed that the PCC of these blocked cells were abnormal in the following respects: (a) some of the G2 PCC were extensively damaged; (b) many of the S PCC failed to incorporate [3H]thymidine; (c) a significant fraction of these PCC were poorly condensed and hence it was difficult to determine whether they were in G1 or G2. These results indicate that there is a good correlation between damage to the genome and the inhibition of cell cycle progression after adriamycin treatment.

The syntheses of 6β-hydroxytestosterone 6-hemisuccinate, 17β-hydroxy-5α-androstane-3,6-dione 6-(O-carboxymethyl) oxime, 11β-hydroxy-19-nortestosterone 11-hemisuccinate, and 11β,17β-dihydroxy-5α-oestran-3-one 11-hemisuccinate are described. The compounds were conjugated with bovine serum albumin in aqueous dioxane by a mixed anhydride procedure and the number of moles of hapten incorporated per mole of albumin was determined.

The preparation of 9alpha, 11xi-tritiated 17alpha-ethinyl estradiol, mestranol, estradiol-17beta, and norethindrone are described. Estrone-3-methyl ether was employed as starting material, and ethinylation with lithium acetylide-ethylene diamine resulted in 95% mestranol. Demethylation of mestranol with boron tribromide at 0 degrees resulted in 92% 17alpha-ethinyl estradiol. Dimethylsulfoxide was the choice of reagent for the condensation reaction which was complete at room temperature in about 4 hours. The usually less than 3% of unreacted 17-oxo product was removed by Girard separation. Demethylation of methyl ether with boran tribromide in methylene chloride resulted in an excellent yield of 17alpha-ethinyl estradiol-9alpha, 11xi-tritium. 3-methoxyestra-1,3,5-trien-17-one-9alpha, 11xi-tritium was reduced with sodium bis(2-methoxyethoxy) aluminum hydride to the 17beta-hydroxy compound and subsequent demethylation resulted in estradiol-9alpha, 11xi-tritium. The general method of Ringold et al was employed for the preparation of 17beta-hydroxy-17alpha-ethinylestr-4-en-3-one. Improvements for small scale radiosynthesis are also presented.

The fate of prematurely condensed chromosomes (PCC) that are induced following fusion between a mitotic and an interphase cell was studied in the homokaryons of HeLa and 2 glycine-requiring mutants of Chinese hamster ovary cells. The data indicate: (1) the prematurely condensed chromosomes are often incorporated into daughter nuclei of the fused cells and hence they are functionally retained by the progeny; (2) in general, the only viable products of fusion between mitotic and interphase cells are those where PCC has been induced; (3) fusion between mitotic and S-phase cells leads to the most rapid loss of chromosomes, while the homophasic fusions tend to produce more stable hybrids with regard to their chromosome number.

A case of unilateral agenesis of tonsil in association with mal-development of the ear has been described. Such an association has not been reported before.

WHEN two mammalian cells fuse and one of the partners is in mitosis while the other is in interphase, the former will induce premature chromosome condensation (PCC) of the latter1. The prematurely condensed chromosomes are considerably longer and thinner than the regular metaphase chromosomes and their morphology reflects the stage of the cell cycle of this interphase nucleus; single chromatid for G1, double chromatids for G2 and unevenly condensed chromatin for S.