Pollen grains in lake sediments: Pollen percentages in surface sediments from southern Michigan

Pollen in surface sediments from five lakes in southern Michigan shows evidence of differential deposition. In most lakes, pollen from ragweed occurs in a higher ratio to tree pollen in shallow-water sediment than in deep water. Pine and certain herbs with small pollen grains follow the same pattern. One very deep lake is an exception, with the ratio of ragweed to tree pollen highest in deep-water sediment. Pollen from local aquatics and from willow, which grows along the lake shore, is also unevenly distributed, occurring in highest frequencies near the parent plants. Pollen from deciduous trees, however, occurs in similar ratios at all sampling stations within each lake. Deciduous pollen occurs in uniform ratios, also in older sediment, deposited in the early 19th century, when the landscape was still forested.Percentages of deciduous tree pollen (as percent tree pollen) were compared among lakes. Single samples were taken for this purpose from the deepest part of each lake basin. Oak pollen percentages are higher in three lakes in western Washtenaw County than in three lakes in eastern Washtenaw County. This difference reflects a similar difference in present-day vegetation: second-growth oak forests grow near the lakes in the western half of the county, while all but 5% of the area in the eastern part of the county is farmland. (The difference in the ratio of farmland to forestland in the two parts of the county is not reflected clearly in the ratio of herb pollen to tree pollen, because there is so much variation within each lake.) In 140-year-old sediment, on the other hand, tree pollen percentages in the six samples are homogeneous as shown by a chi-square test. The homogeneity in sediment deposited before the forest was cleared is surprising, because witness-tree data from presettlement time show that the frequencies of tree species in the two areas were quite different. Pollen dispersal at that time must have been effective enough, to counteract differences over distances of a few tens of kilometers in the amounts and kinds of pollen produced by the vegetation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/33513/1/0000011.pd

Strategies for Gait Retraining in a Collegiate Runner with Transfemoral Amputation: A Case Report

# Background More than fifty percent of people with limb amputations participate in sports or physical activity following amputation. Athletes with limb amputations may face additional challenges including phantom limb pain (PLP), psychological barriers, prosthetic complications, and gait abnormalities. Prevalence of PLP in the general amputee population is estimated to be as high as 85%. Despite the high prevalence of PLP, there is little research regarding the use of gait training as a treatment for PLP among both the general amputee population and athletes. # Case Description A 20-year old female collegiate track and field athlete presented with phantom knee pain brought on with running. The athlete demonstrated deficits in core and hip strength as well as decreased single leg stability bilaterally. Running gait analysis revealed circumduction with the prosthesis for limb advancement and increased vaulting with push off on the sound (uninvolved) limb. Gait retraining strategies were implemented to address video analysis findings and create a more efficient running gait and address phantom limb pain symptoms. # Outcomes Rehabilitation and gait retraining strategies were effective in improving several clinical and functional outcomes in this case. Significant improvements were noted in PLP, running gait mechanics, and the patient’s psychological and functional status as measured with a standardized outcome tool, the Patient-Reported Outcomes Measurement Information System^®^ (PROMIS^®^). # Discussion Running gait training following amputation could be a crucial component of rehabilitation for athletes in an attempt to lessen pain while running, especially in those experiencing phantom limb pain (PLP). Utilization of a multidisciplinary team in the gait retraining process is recommended. There is a need for further research to determine the effects of running gait retraining for management of PLP in athletes with amputation. # Level of Evidence

Characterisation of a Peripheral Neuropathic Component of the Rat Monoiodoacetate Model of Osteoarthritis

Joint degeneration observed in the rat monoiodoacetate (MIA) model of osteoarthritis shares many histological features with the clinical condition. The accompanying pain phenotype has seen the model widely used to investigate the pathophysiology of osteoarthritis pain, and for preclinical screening of analgesic compounds. We have investigated the pathophysiological sequellae of MIA used at low (1 mg) or high (2 mg) dose. Intra-articular 2 mg MIA induced expression of ATF-3, a sensitive marker for peripheral neuron stress/injury, in small and large diameter DRG cell profiles principally at levels L4 and 5 (levels predominated by neurones innervating the hindpaw) rather than L3. At the 7 day timepoint, ATF-3 signal was significantly smaller in 1 mg MIA treated animals than in the 2 mg treated group. 2 mg, but not 1 mg, intra-articular MIA was also associated with a significant reduction in intra-epidermal nerve fibre density in plantar hindpaw skin, and produced spinal cord dorsal and ventral horn microgliosis. The 2 mg treatment evoked mechanical pain-related hypersensitivity of the hindpaw that was significantly greater than the 1 mg treatment. MIA treatment produced weight bearing asymmetry and cold hypersensitivity which was similar at both doses. Additionally, while pregabalin significantly reduced deep dorsal horn evoked neuronal responses in animals treated with 2 mg MIA, this effect was much reduced or absent in the 1 mg or sham treated groups. These data demonstrate that intra-articular 2 mg MIA not only produces joint degeneration, but also evokes significant axonal injury to DRG cells including those innervating targets outside of the knee joint such as hindpaw skin. This significant neuropathic component needs to be taken into account when interpreting studies using this model, particularly at doses greater than 1 mg MIA

Role for corticoids in mediating the response of Rana pipiens tadpoles to intraspecific competition

Competition is known to decrease growth and development rate in tadpoles, but the physiological basis for this phenomenon is poorly understood. We hypothesized that competition results in increased production of stress hormones and that these hormones are responsible for the suppression of growth and development. To test this hypothesis, we measured whole-body corticosterone content in premetamorphic Leopard frog ( Rana pipiens ) tadpoles raised at two different population densities and three different food levels. Whole body corticosterone content was elevated in tadpoles subjected to either limited food (at low density) or high density. Within the low and intermediate food treatments, high density reduced tadpole growth and slowed development. Limited food slowed growth and development at all densities. Blocking corticoid synthesis by treating tadpoles with metyrapone (MTP) reversed the growth suppression caused by high density (tested in the intermediate food level treatment) but did not alter the effect of density on development rate. MTP treatment did not alter the depressive effect of limited resources on growth or development. Our results suggest that elevated corticoid biosynthesis mediates the negative effect of increased population density (i.e., increased intraspecific competition) on tadpole growth. J. Exp. Zool. 292:32–40, 2002 . © 2002 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34473/1/1140_ftp.pd

Epidermal innervation and thermal nociception in rodent models of diabetic neuropathy

The assessment of epidermal innervation is emerging as a valuable means of diagnosing and staging clinical diabetic neuropathy. In order to address whether or not rodent models of diabetes develop a similar loss of cutaneous innervation, we quantified epidermal nerve fiber density in various strains of diabetic rats and mice. After confirming that each of these strains developed epidermal nerve fiber loss, as well as epidermal thinning, we examined the relationship between changes in epidermal nerve fiber density and changes in heat sensitivity. After 2 weeks of diabetes, Swiss Webster mice developed significant thermal hypoalgesia. However, a significant reduction in epidermal innervation did not develop until after 4 weeks of diabetes, indicating that loss of heat sensitivity precedes a detectable reduction in epidermal innervation. Next we attempted to examine the mechanisms of thermal hypoalgesia by examining the effects of an aldose reductase inhibitor and exogenous neurotrophic support in type 1 diabetic Swiss Webster mice. The aldose reductase inhibitor IDD 676 and the NGF-enhancing compound Neotrofin partially ameliorated motor nerve conduction velocity slowing, but were unable to prevent thermal hypoalgesia. CNTF and the prosaposin-like peptide TX14(A) prevented the development of thermal hypoalgesia, but none of these compounds were able to reverse established deficits. Next we examined the neurotrophic properties of insulin by comparing the severity of neuropathy in type 1 and type 2 diabetic mouse models. Both models developed thermal hypoalgesia and IENF deficits, indicating that insulin does not protect against the development of these deficits. To further explore insulin's neurotrophic properties, we examined the effects of insulin supplementation in a type 1 diabetic mouse model. Low doses of insulin prevented epidermal thinning after 4 weeks of diabetes and high doses of insulin prevented thermal hypoalgesia after 4 and 8 weeks of diabetes, indicating neurotrophic effects of insulin. Together, these results demonstrate that rodent models develop the epidermal nerve fiber loss observed in humans with diabetes. However, a loss of thermal sensitivity precedes reductions in epidermal innervation. Loss of neurotrophic support may be involved in the development of these deficit