Zinc Deficiency and Anther Development in Maize

With the onset of male reproductive phase at 28 days, zinc waswithdrawn from fifty percent of maize (Zea mays L. cv. Ganga2) plants grown in refined sand at 0.13 mg Zn liter^–1.Plants from which zinc was withdrawn developed zinc deficiencysymptoms in young leaves after 38 days and were low in tissuezinc. Their tassel formation and pollen development was retarded.Anthers failed to develop beyond freshly liberated young pollengrain stage and vessels were formed in place of sporogenoustissue in sixty percent anthers of the younger of the two florets.Anthers from these plants showed low zinc concentration andstimulated specific activities of catalase, peroxidase, ribonucleaseand acid phosphatase. On resuming normal zinc (0.13 mg Zn liter^–1) through rootsto the plants from which it was withdrawn for 17 days, vegetativegrowth was partially renewed and short axillary buds were formedbut the development of anthers remained retarded. (Received April 11, 1986; Accepted October 15, 1986)     

Molybdenum nutrition of isolates of four Aspergillus species

The molybdenum requirement for growth and conidial formation by Aspergillus flavus, A. terreus, and A. sulphureus was found to be 0.2 ppb, which was one-fifth that of an A. niger isolate. Molybdenum deficiency depressed growth, conidial formation, dry weight, soluble protein, and the specific activities of nitrate reductase, succinic dehydrogenase, and aconitase in all the isolates of Aspergillus studied, but the specific activities of catalase and peroxidase were depressed only in isolates of A. niger, A. terreus, and A. flavus. Also, molybdenum deficiency stimulated the specific activities of acid phosphatase and ribonuclease in the A. flavus isolate, although the specific activities of these enzymes decreased in other isolates. Eighteen hours after the addition of molybdenum (5 ppb) to molybdenum-deficient (0.02 ppb) cultures of A. niger, the specific activities of catalase, peroxidase and succinic dehydrogenase were restored in the absence of cycloheximide, while the specific activity of nitrate reductase was recovered even in the presence of the inhibitor. There was no effect on the specific activities of aconitase and acid phosphatase following the addition of molybdenum to molybdenum-deficient cultures of A. niger.     

Correlation of encystment and division in Schizopyrenus russelli.

Schizopyrenus russelli, a free-living soil ameba, grows and encysts in the presence of bacteria. The encystment occurs with decline in the division rate. This is accompanied by incorporation of [U-14C] glucose into cyst cellulose. The degree of multiplication (but not of encystment) is a function of bacterial concentration. Berenil, a trypanocidal drug, while allowing excystment, completely inhibited multiplication of emerged amebae and their encystment. Addition of this drug after 24 hr, when amebae had gone into a phase of active division failed to check encystment, although it still inhibited further multiplication of the amebae. The findings suggest that a phase of cell division may be a prerequisite for encystment.     

In-Silico Repurposing of Anticancer Drug (5-FU) as an Antimicrobial Agent Against Methicillin-Resistant Staphylococcus aureus (MRSA)

International Journal of Peptide Research and Therapeutics - The Centers for Disease Control and Prevention (CDC) reported earlier that more than 11,000 people died from a methicillin-resistant...     

Partial Restoration of Macrophage Alteration from Diet-Induced Obesity in Response to Porphyromonas gingivalis Infection

Obesity is a chronic inflammatory disease that weakens macrophage innate immune response to infections. Since M1 polarization is crucial during acute infectious diseases, we hypothesized that diet-induced obesity inhibits M1 polarization of macrophages in the response to bacterial infections. Bone marrow macrophages (BMMΦ) from lean and obese mice were exposed to live Porphyromonas gingivalis (P. gingivalis) for three incubation times (1 h, 4 h and 24 h). Flow cytometry analysis revealed that the M1 polarization was inhibited after P. gingivalis exposure in BMMΦ from obese mice when compared with BMMΦ from lean counterparts. Using a computational approach in conjunction with microarray data, we identified switching genes that may differentially control the behavior of response pathways in macrophages from lean and obese mice. The two most prominent switching genes were thrombospondin 1 and arginase 1. Protein expression levels of both genes were higher in obese BMMΦ than in lean BMMΦ after exposure to P. gingivalis. Inhibition of either thrombospondin 1 or arginase 1 by specific inhibitors recovered the M1 polarization of BMMΦ from obese mice after P. gingivalis exposure. These data indicate that thrombospondin 1 and arginase 1 are important bacterial response genes, whose regulation is altered in macrophages from obese mice.     

Mechanisms underlying ischemic diastolic dysfunction: relation between rigor,calcium homeostasis,and relaxation rate

Increased diastolic chamber stiffness (upward arrow DCS) during ischemia may result from increased diastolic calcium, rigor, or reduced velocity of relaxation. We tested these potential mechanisms during severe ischemia in isolated red blood cell-perfused isovolumic rabbit hearts. Ischemia (coronary flow reduced 83%) reduced left ventricular (LV) contractility by 70%, which then remained stable. DCS progressively increased. When LV end-diastolic pressure had increased 5 mmHg, myofilament calcium responsiveness was altered with 50 mmol/l NH(4)Cl or 10 mmol/l butanedione monoxime. These affected contractility (i.e., a calcium-mediated force) but not upward arrow DCS. Second, quick length changes reversed upward arrow DCS, supporting a rigor mechanism. Third, ischemia increased the time constant of isovolumic pressure decline from 47 +/- 3 to 58 +/- 3 ms (P < 0.02) but concomitantly abbreviated the contraction-relaxation cycle, i.e., pressure dissipation occurred earlier without diastolic tetanization. Finally, to assess any link between rate of relaxation and upward arrow DCS, hearts were exposed to 10 mmol/l calcium. Calcium doubled contractility and accelerated relaxation velocity, but without affecting upward arrow DCS. Thus upward arrow DCS developed during ischemia despite severely reduced contractility via a rigor (and not calcium mediated) mechanism. Calcium resequestration capacity was preserved, and reduced relaxation velocity was not linked to upward arrow DCS.