Citations

The biomechanical evaluation of patients with painful heels has received only limited attention although the potential morbidity and disability associated with such an ailment can be severe. An objective analysis of the patient's foot function during gait can produce useful information to assess the underlying pathology. This method can also help to evaluate the efficacy of various existing treatment protocols. The impulse distribution based on foot-floor vertical reaction force and time under the hind-, mid-, and forefoot was determined in 32 normal subjects while walking in their usual street shoes. Variations related to shoe types were noted, with high heeled shoes causing the most significant deviations from normal. The same technique was applied to 13 painful heel syndrome patients. Characteristic deviations from the normal impulse distribution were noted in these patients which provided the basis for differentiating the pathological condition between the patients with painful heel pads and those with plantar fasciitis. The effectiveness of using heel cups as a therapeutic device was also assessed. Although significant gait changes were not associated with the insertion of heel cups, they did seem to shift the foot-floor impulse forward from the heel region, which made them effective in patients afflicted with localized heel pain, but not in those with plantar fasciitis.

Eleven patients who were treated for talonavicular arthrosis with a talonavicular arthrodesis between 1961 and 1979 at the Mayo Clinic have been reviewed. Follow-up from surgery ranged from 2.5 to 21 years with a mean of 9.5 years. Clinical, radiographic, and gait analyses were obtained. All patients had satisfactory pain relief, but all noted difficulty in ambulating on irregular ground. Three patients had roentgenographic evidence of arthrosis affecting other tarsal joints that had not been involved before arthrodesis. Gait analysis revealed decreased terminal stance-phase plantarflexion and pronounced reduction of subtalar motion. Talonavicular arthrodesis does give predictable union and patient satisfaction but results in limitation of subtalar motion and loss of stance-phase plantarflexion.

In spite of the common occurrence of pes planus and multiple operations that have been reported to relieve the associated symptoms, there is little published on the relative contribution of various structures to stabilization of the arch of the foot. Twelve fresh-frozen human cadaveric feet were loaded along the tibial axis with compressive loads of 230, 460, and 690 newtons with the specimens intact and after sequential sectioning of plantar fascia, plantar ligaments, and spring ligament. Structures were sectioned in six different sequences and changes in vertical and horizontal dimensions of the medial arch were measured. The highest relative contribution to arch stability was provided by the plantar fascia, followed by plantar ligaments and spring ligament. Plantar fascia was a major factor in maintenance of the medial longitudinal arch. Its division in the cadaveric feet decreased arch stiffness by 25%.

Implant removal and synovectomy were used to treat the failure of 14 first metatarsophalangeal joint implant arthroplasties. Revision surgery was performed at an average of 3.1 years after arthroplasty. Follow-up (average 4.9 years) was possible in 10 patients, and clinical results were excellent in seven patients, good in one patient, fair in one patient, and poor in one patient. No significant changes in alignment occurred, although a trend toward toe extension was noted. Dynamic force plate studies in these patients demonstrated less pressure under the first metatarsal head and greater loading under the lateral forefoot. The great toe had less contact time during gait in the involved feet than in the control feet.

Thirteen consecutive patients underwent plantar fasciotomy in 16 feet for intractable plantar fasciitis and had follow-up from 4.5 to 15 years. Plantar fasciotomy was successful (good or excellent results) for 71% of the 14 feet operated on and for which follow-up data were available. However, time to full recovery was prolonged, additional treatment was frequently required, and abnormalities of foot function persisted. Flattening of the longitudinal arch occurred. Dynamic force-plate studies showed differences in peak vertical, fore-aft, and lateralmedial forces between patients and matched controls. More rapid progression of weightbearing along the longitudinal axis of the foot during stance phase in patients indicated avoidance of heel loading.

The objective documentation of foot function before and after therapeutic intervention will be greatly enhanced by the utilization of devices capable of measuring dynamic foot pressure distribution. Efforts to develop this technology date back to the late 19th century, but only with recent advances in computers has it been possible to produce quantitatively accurate high resolution foot pressure distribution with high sampling rates and easily interpreted graphic displays. Over the years, a variety of methods have been employed to study foot pressure. Many of these techniques have already improved our understanding of the foot and its function, and have had an impact on the way we practice. Effective clinical utilization of these new investigative tools depends on an understanding of their scientific basis, capabilities and limitations.

Objective— Endothelial cell (EC) inflammatory status is critical to many vascular diseases. Emerging data demonstrate that mutations of Krüppel-like factor-11 (KLF11), a gene coding maturity-onset diabetes mellitus of the young type 7 ( MODY7 ), contribute to the development of neonatal diabetes mellitus. However, the function of KLF11 in the cardiovascular system still remains to be uncovered. In this study, we aimed to investigate the role of KLF11 in vascular endothelial inflammation. Methods and Results— KLF11 is highly expressed in vascular ECs and induced by proinflammatory stimuli. Adenovirus-mediated KLF11 overexpression inhibits expression of tumor necrosis factors-α–induced adhesion molecules. Moreover, small interfering RNA–mediated KLF11 knockdown augments the proinflammatory status in ECs. KLF11 inhibits promoter activity of adhesion molecules induced by tumor necrosis factor-α and nuclear factor-κB p65 overexpression. Mechanistically, KLF11 potently inhibits nuclear factor-κB signaling pathway via physical interaction with p65. Furthermore, KLF11 knockdown results in increased binding of p65 to vascular cell adhesion molecule-1 and E-selectin promoters. At the whole organism level, KLF11 −/− mice exhibit a significant increase in leukocyte recruitment to ECs after lipopolysaccharide administration. Conclusion— Taken together, our data demonstrate for the first time that KLF11 is a suppressor of EC inflammatory activation, suggesting that KLF11 constitutes a novel potential molecular target for inhibition of vascular inflammatory diseases.

Described for the first time in 1971, Schimke immuno-osseous dysplasia (SIOD) is an autosomal-recessive multisystem disorder that is caused by bi-allelic mutations of SMARCAL1, which encodes a DNA annealing helicase. To define better the dental anomalies of SIOD, we reviewed the records from SIOD patients with identified bi-allelic SMARCAL1 mutations, and we found that 66.0% had microdontia, hypodontia, or malformed deciduous and permanent molars. Immunohistochemical analyses showed expression of SMARCAL1 in all developing teeth, raising the possibility that the malformations are cell-autonomous consequences of SMARCAL1 deficiency. We also found that stimulation of cultured skin fibroblasts from SIOD patients with the tooth morphogens WNT3A, BMP4, and TGFβ1 identified altered transcriptional responses, raising the hypothesis that the dental malformations arise in part from altered responses to developmental morphogens. To the best of our knowledge, this is the first systematic study of the dental anomalies associated with SIOD.

The present study determined circulating concentrations of atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP) in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) and also investigated the vasorelaxing action of ANP and CNP on isolated contracted aorta. We also defined the vasorelaxing action of a novel and newly synthesized 27-amino acid chimera of ANP and CNP termed vasonatrin peptide (VNP), which we compared with ANP and CNP in WKY rats and SHR. Plasma and urinary cyclic GMP and sodium excretion were also investigated. Plasma ANP was increased in SHR in contrast to no change in circulating CNP. Plasma and urinary cyclic GMP and sodium excretion were no different between WKY rats and SHR. In WKY rats maximal relaxations to VNP in aortic rings without endothelium were greater than those to ANP and CNP. In SHR aortic rings the potency of VNP relaxation was preserved, the actions of ANP were enhanced, and the actions of CNP were markedly impaired. In association with these vasorelaxing actions, these data suggest that (1) circulating CNP is not different in SHR and WKY rats, but the aortic relaxing action of CNP is markedly impaired in SHR; (2) endogenous plasma ANP is significantly increased in SHR without associated increases in plasma or urinary cyclic GMP; (3) there is an increase in aortic relaxation to exogenous ANP in SHR; and (4) VNP has a potent endothelium-independent aortic relaxing action in both WKY rats and SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic peptide is an important peptide hormone of cardiac origin that functions to regulate cardiac preload via the regulation of sodium excretion. This natriuretic action occurs through activation of the particulate guanylyl cyclase-linked natriuretic peptide-A receptor. HS-142-1 is a newly discovered antagonist of the natriuretic peptide-A receptor that permits insight into the functional role of atrial natriuretic peptide in cardiorenal homeostasis. The first objective of this study was to define for the first time the intrarenal action of HS-142-1 on exogenous atrial natriuretic peptide-mediated natriuresis in anesthetized normal dogs. In group 1 (n = 6), which received intravenous atrial natriuretic peptide at 100 ng/kg per minute, intrarenal HS-142-1 (0.5 mg/kg bolus) attenuated atrial natriuretic peptide-induced increases in glomerular filtration rate, urine flow, sodium excretion, and renal cyclic GMP generation and decreases in distal tubular sodium reabsorption. The second objective was to determine whether endogenous atrial natriuretic peptide participates in the regulation of basal sodium excretion. In group 2 (n = 6), intrarenal HS-142-1 alone decreased both absolute and fractional sodium excretion and renal cyclic GMP generation and increased distal tubular sodium reabsorption. These studies demonstrate that HS-142-1 markedly attenuates exogenous atrial natriuretic peptide-mediated natriuresis via enhancement of distal tubular reabsorption and blunting of increases in glomerular filtration rate. Second, the current studies support a functional role for endogenous atrial natriuretic peptide in the regulation of basal sodium excretion.