Effects of Herding on Rangeland Use Efficiency in Kenya

Within each foraging itinerary, herders can intervene in the forage selection process, encouraging herds to use highly palatable and less palatable rangeland resources. Such a herding strategy could prevent rangeland degradation and increase livestock productivity. The objectives of this study were to examine forage availability and identify factors influencing stocking rates around night resting places on a ranch in Laikipia County, Kenya. Forage availability was measured along six regularly spaced transects around night resting places corralling one herd of camels, one mixed herd of goats and sheep, and two herds of cattle, with biomass sampling points at 50-, 150-, 250-, and 350-meter distance from the night resting places. Every four days, herbaceous biomass was collected at each sampling point and classified into monocotyledonous plants, dicotyledonous plants, and litter. Pooled samples of biomass were analyzed for their nutrient content. Activities of herders and herds were monitored. Stocking rates were calculated for the sampling points using georeferenced data of foraging itineraries recorded in 20-second intervals, area densities of herds measured by a hand-held global positioning system receiver, and live weights of all animals determined monthly. Except for the herd of camels, the distance to the night resting places had no effect on stocking rates. Not forage nutritive value, but palatability of dominant species on sampling points mainly influenced stocking rates, and thus forage availability. All livestock species sought patches dominated by Cynodon dactylon, possibly being overgrazed. Patches dominated by either Andropogon contortus or Themeda triandra were underused, as indicated by biomass accumulation. Thus, the efforts of the hired herders in this study did not lead to the desired herding effects. Therefore, motivating herders to design foraging itineraries utilizing diverse vegetation patches intentionally is crucial to an efficient use of rangeland resources, while meeting the nutritional requirements of animals

Impact of ambient air filters on PM concentration levels at an urban traffic hotspot (Stuttgart, Am Neckartor)

Air pollution can have severe impacts on public health. A novel approach to lower the local particle concentrations at urban hotspots is ambient air filtration. This study presents experimental investigations into the effectiveness of air filters to lower ambient particle concentration levels at two different locations. Seventeen outdoor filtration devices with a total flow rate of 170.000 m³/h were installed beside federal highway B14 at Stuttgart “Am Neckartor” targeting to reduce PM10 concentration levels within a 300 m × 50 m area around the urban pollution hotspot. Further measurements were conducted at the residential area “Bleyle quarter” to show the capabilities of a single filter device under relatively defined conditions. By periodically switching the filters on and off while monitoring the particle mass concentrations with optical particle counters, the effects of the filters on the PM10 and PM2.5 concentration levels were determined. A long term investigation at the Neckartor installation site (466 h) yielded an average PM10 reduction of 10.4% (6.3 μg/m³) at the official Neckartor measurement station. Additional in situ measurement campaigns showed that the PM reduction effect decreases with increasing distance to the filter devices. However, the effect is clearly measurable in the walkway areas across the installation site

A rapid staining technique for the detection of the initiation of germination of bacterial spores

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75645/1/j.1472-765x.2002.01047.x.pd

EAST/SeSAME Syndrome and Beyond: The Spectrum of Kir4.1- and Kir5.1-Associated Channelopathies

In 2009, two groups independently linked human mutations in the inwardly rectifying K+ channel Kir4.1 (gene name KCNJ10) to a syndrome affecting the central nervous system (CNS), hearing, and renal tubular salt reabsorption. The autosomal recessive syndrome has been named EAST (epilepsy, ataxia, sensorineural deafness, and renal tubulopathy) or SeSAME syndrome (seizures, sensorineural deafness, ataxia, intellectual disability, and electrolyte imbalance), accordingly. Renal dysfunction in EAST/SeSAME patients results in loss of Na+, K+, and Mg2+ with urine, activation of the renin–angiotensin–aldosterone system, and hypokalemic metabolic alkalosis. Kir4.1 is highly expressed in affected organs: the CNS, inner ear, and kidney. In the kidney, it mostly forms heteromeric channels with Kir5.1 (KCNJ16). Biallelic loss-of-function mutations of Kir5.1 can also have disease significance, but the clinical symptoms differ substantially from those of EAST/SeSAME syndrome: although sensorineural hearing loss and hypokalemia are replicated, there is no alkalosis, but rather acidosis of variable severity; in contrast to EAST/SeSAME syndrome, the CNS is unaffected. This review provides a framework for understanding some of these differences and will guide the reader through the growing literature on Kir4.1 and Kir5.1, discussing the complex disease mechanisms and the variable expression of disease symptoms from a molecular and systems physiology perspective. Knowledge of the pathophysiology of these diseases and their multifaceted clinical spectrum is an important prerequisite for making the correct diagnosis and forms the basis for personalized therapies

Loss of aquaporin-4 expression and putative function in non-small cell lung cancer

<p>Abstract</p> <p>Background</p> <p>Aquaporins (AQPs) have been recognized to promote tumor progression, invasion, and metastasis and are therefore recognized as promising targets for novel anti-cancer therapies. Potentially relevant AQPs in distinct cancer entities can be determined by a comprehensive expression analysis of the 13 human AQPs.</p> <p>Methods</p> <p>We analyzed the presence of all AQP transcripts in 576 different normal lung and non-small cell lung cancer (NSCLC) samples using microarray data and validated our findings by qRT-PCR and immunohistochemistry.</p> <p>Results</p> <p>Variable expression of several AQPs (AQP1, -3, -4, and -5) was found in NSCLC and normal lung tissues. Furthermore, we identified remarkable differences between NSCLC subtypes in regard to AQP1, -3 and -4 expression. Higher transcript and protein levels of AQP4 in well-differentiated lung adenocarcinomas suggested an association with a more favourable prognosis. Beyond water transport, data mining of co-expressed genes indicated an involvement of AQP4 in cell-cell signalling, cellular movement and lipid metabolism, and underlined the association of AQP4 to important physiological functions in benign lung tissue.</p> <p>Conclusions</p> <p>Our findings accentuate the need to identify functional differences and redundancies of active AQPs in normal and tumor cells in order to assess their value as promising drug targets.</p

A Novel Y152C KCNJ5 Mutation Responsible for Familial Hyperaldosteronism Type III

CONTEXT: Primary aldosteronism is a heterogeneous group of disorders comprising both sporadic and familial forms. Mutations in the KCNJ5 gene, which encodes the inward rectifier K(+) channel 4 (G protein-activated inward rectifier K(+) channel 4, Kir3.4), cause familial hyperaldosteronism type III (FH-III) and are involved in the pathogenesis of sporadic aldosterone-producing adenomas. OBJECTIVE: The objective of the study was to characterize the effects of a newly described KCNJ5 mutation in vitro. PATIENTS AND METHODS: The index case is a 62-year-old woman affected by primary aldosteronism, who underwent left adrenalectomy after workup for adrenal adenoma. Exon 1 of KCNJ5 was PCR amplified from adrenal tissue and peripheral blood and sequenced. Electrophysiological and gene expression studies were performed to establish the functional effects of the new mutation on the membrane potential and adrenal cell CYP11B2 expression. RESULTS: KCNJ5 sequencing in the index case revealed a new p.Y152C germline mutation; interestingly, the phenotype of the patient was milder than most of the previously described FH-III families. The tyrosine-to-cysteine substitution resulted in pathological Na(+) permeability, cell membrane depolarization, and disturbed intracellular Ca(2+) homeostasis, effects similar, albeit smaller, to the ones demonstrated for other KCNJ5 mutations. Gene expression studies revealed an increased expression of CYP11B2 and its transcriptional regulator NR4A2 in HAC15 adrenal cells overexpressing KCNJ5(Y152C) compared to the wild-type channel. The effect was clearly Ca(2+)-dependent, because it was abolished by the calcium channel blocker nifedipine. CONCLUSIONS: Herein we describe a new germline mutation in KCNJ5 responsible for FH-III