Agility through discipline: a debate

While Beck asserts that agility is only possible through greater discipline on the part of everyone involved, Boehm counters that you don't broaden the definition of "discipline" by rejecting parts of it. Yet, from inside extreme programming, it seems that the only way to achieve the desired results is to view the world in 'both-and" terms instead of "either-or" terms.     

Dynamic thermographic imaging for estimation of regional perfusion in the tuberculin reaction in healthy adults

A sensitive method for measurement of the volume of blood flow through the skin, based on the kinetics of reheating after localised cooling, is described in this paper. This method has been used to study the tuberculin reaction as a model of cutaneous delayed-type hypersensitivity (DHS) in man. Over the positive reaction there is accelerated reheating similar in kinetics and extent to that seen after maximal hyperaemia induced by intradermal injection of histamine or prostaglandin E2. The earlier phase of reheating (10-100 s) is more dependent on blood flow, whereas the later phase (100-300 s) is apparently more dependent on non-perfusion heat exchange mechanisms, including conduction. The reheat kinetic method is largely dependent on blood flow in the deep dermal vessels (diameter > 50 microns), whereas the alternative approach of measurement of the velocity of flow of erythrocytes in the microcirculation by laser Doppler (LD) flowmetry gives results biased towards the most superficial dermal circulation. Previous studies with LD flowmetry have shown that the blood velocity is greatest at the centre of weak and strong reactions, while in the most intense reactions it is raised at the centre but maximal at the periphery (central relative slowing, CRS) raising the possibility of central ischaemia. The reheat kinetics approach has now indicated that the deep dermal circulation is not impaired in CRS reactions. It is concluded that there must be partial obstruction of the parts of the microcirculation communicating between the deep and superficial dermal plexuses, presumably from the accumulation of exudate oedema in the most intense tuberculin reactions.     

CMOS on FZ-high resistivity substrate for monolithic integration ofSiGe-RF-circuitry and readout electronics

The choice of a highly resistive substrate for silicon millimeter-wave integrated circuits (SIMMWIC) imposed by the requirement of low RF-substrate losses requires the adaptation of a CMOS process on float zone silicon (FZ). A comparison of n- and p-channel devices realized on high resistivity substrate (p-type, 5000 Ω·cm) and standard CMOS substrates (CZ, n-type, 4-6 Ω·cm) is given. Using careful process design, we obtained device characteristics on FZ-substrates that are closely similar to those on standard material, thus allowing direct transfer of existing circuit designs     

Modeling phosphorus in the upper Etowah River basin: identifying sources under uncertainty.

The Uniform Covering by Probabilistic Rejection (UCPR) algorithm was used, in conjunction with the Soil and Water Assessment Tool (SWAT) model, to identify P loads from point source and nonpoint source polluters in the upper Etowah River basin (UERB) in Georgia. The key findings of the research are as follows. The mean absolute error was preferred over the root mean square error as a search criterion for the UCPR algorithm when water quality observations are scarce. The undocumented P load from point sources in the UERB was consistently estimated as about 43 kg/d by the proposed method; but the method was not able to identify the broiler litter application rate to the poultry/beef operation pastures. Point sources (both documented and undocumented), poultry/beef operation pastures, and forests are the three major contributors of P. During 1992-1996, on average they accounted for 36.4, 31.7, and 17.2% of P load from the UERB, respectively.     

Single-strand conformational polymorphism analysis of the M(r) 170,000 isozyme of DNA topoisomerase II in human tumor cells

Five cell lines selected for resistance to the cytotoxicity of inhibitors of DNA topoisomerase II have point mutations in the gene that codes for the M(r) 170,000 form of this enzyme. In each case, the mutation results in an amino acid change in or near an ATP binding sequence of the M(r) 170,000 isozyme of topoisomerase II. We used single-strand conformational polymorphism analysis to screen for similar mutations in other drug-resistant cell lines or in leukemic cells from patients previously treated with etoposide or teniposide. We also analyzed the region of the gene that codes for amino acids adjacent to the tyrosine at position 804 of topoisomerase II which binds covalently to DNA. CEM/VM-1, CEM/VM-1-5, and HL-60/AMSA human leukemic cell lines were used as controls; 3 of 3 known mutations were detected by migration differences of polymerase chain reaction products from the RNA extracted from these three lines. A previously unknown mutation was found in the tyrosine 804 region of the M(r) 170,000 topoisomerase II expressed by CEM/VM-1 and CEM/VM-1-5 cells. Sequence analysis showed that substitution of a T for a C at nucleotide 2404 resulted in an amino acid change of a serine for a proline at amino acid 802. No mutations in any of the ATP binding sequences or in the tyrosine 804 region were detected in polymerase chain reaction products from RNA extracted from human leukemia HL-60/MX2 or CEM/MX1 cells (both cell lines selected for resistance to mitoxantrone) or in human myeloma 8226/Dox1V cells (selected for resistance by simultaneous exposure to doxorubicin and verapamil). No mutations were detected in polymerase chain reaction products from RNA extracted from blasts of 15 patients with relapsed acute lymphocytic leukemia, previously treated with etoposide or teniposide. We conclude that: (a) single-strand conformational polymorphism analysis is useful for screening for mutations in topoisomerase II; (b) resistance to the cytotoxicity of inhibitors of DNA topoisomerase II is not always associated with mutations in ATP binding sequences or the active site tyrosine region of M(r) 170,000 topoisomerase II; and (c) mutations similar to those detected in drug resistant cells selected in culture have not been identified in blast cells from patients with relapsed acute lymphocytic leukemia, previously treated with etoposide or teniposide.