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Background: Although considerable literature can be found on the outcome of total ankle replacement (TAR), only a few studies have reported the results of the fixed-bearing Cadence prosthesis. This noninventor study reports a consecutive series of 60 Cadence TAR systems with a mean of 2.9 years’ follow-up, focusing on clinical and radiographic outcomes and early complications. This study is the first to assess true postoperative radiographic ankle prosthesis range of motion (ROM) and to report an unanticipated serious adverse device effect. Methods: Sixty patients who underwent primary TAR with the Cadence prosthesis between July 2016 and July 2019 were clinically and radiographically evaluated preoperatively and at last follow-up after the procedure. Revisions, additional procedures, implant failure, and complications were reported according to the classifications of Vander Griend and Glazebrook. Radiographic outcomes included radiographic TAR ROM, bone-implant interface, and alignment parameters. Results: The survival rate of the prosthesis was 98.3%. The mean radiographic ankle ROM at the last follow-up was 24 degrees (9 degrees of dorsiflexion and 15 degrees of plantarflexion). The coronal and sagittal alignment of TAR was 90.8 degrees and 3.9 degrees, respectively. Bone-implant interface analysis revealed osteolysis in 9 ankles (15%) and radiolucent lines in 33 ankles (55%) occurring at both component interfaces. Intraoperative complications were 3 periprosthetic malleolar fractures (5%). Five talar implant fractures (implant failure of 8.3%) were observed, and 1 unexplained persistent pain that required a conversion from TAR to a tibiotalocalcaneal arthrodesis. Conclusion: Clinical, radiograph ROM, implant position outcomes, and survival rate at an early-term follow-up of 2.9 years were similar to those reported in recent Cadence studies. However, this study reports 5 unanticipated talar implant fractures and a high rate of posterior radiolucent lines. Level of evidence: Level IV, retrospective case series.

Clinical and cadaver studies have reported that supernumerary muscles could be the etiology of a variety of pathologic disorders, such as posterior impingement syndrome, tarsal tunnel syndrome (TTS), and flexor hallucis longus tenosynovitis. We describe a unique variant of the flexor digitorum accessorius longus (FDAL) muscle as an apparent cause of TTS, functioning as an independent flexor of the second toe, which has not been described in the literature. In addition to this case report, a systematic review was performed of TTS caused by the FDAL muscle.A targeted search of PubMed, the Cochrane Library, the Cumulative Index to Nursing and Allied Health Literature, and Web of Science identified full-text papers that fulfilled the inclusion and exclusion criteria.Twenty-nine papers were identified for inclusion in the systematic review: 12 clinical papers of TTS caused by the FDAL muscle and 17 cadaver-based papers.Clinicians often do not include the FDAL muscle in the differential diagnosis of TTS. This literature review suggests that the FDAL is an important muscle in terms of its functional and clinical significance. Knowledge of this muscle, its anatomical location and variations, and its magnetic resonance imaging characteristics may help clinicians make an accurate differential diagnosis.

Iatrogenic hallux varus is a possible complication of hallux valgus surgery following Mc Bride or Scarf osteotomy, with or without Akin osteotomy of the first phalanx. It may also occur following chevron osteotomy or Keller's procedure. One possibility for surgical revision of iatrogenic hallux varus is reconstruction of the lateral stabilising soft-tissue components of the first metatarsophalangeal joint. Until now, only dynamic tendon transfers, possibly combined with interphalangeal fusion, have been described. The aim of our study was to develop a static, anatomic reconstruction procedure. A new surgical technique of ligamentoplasty using the abductor hallucis tendon is described. The new method was applied in 7 feet (5 patients) with a mean follow-up over two years. Hallux varus deformities were operated by transplantation of the abductor hallucis tendon. Subsequent radiographs showed correction of most of the factors considered to be responsible for the iatrogenic deformity. The American Orthopaedic Foot and Ankle Society (AOFAS) hallux metatarsophalangeal-interphalangeal (MTP-IP) score improved from 61 to 88. This new technique is a reliable, anatomic reconstruction with use of the tendon involved in the pathogenesis of the hallux varus deformity. No other functional tendon is used.

The urinary excretion of beta 2-microglobulin, retinol-binding protein and albumin was measured in 65 workers exposed to styrene at levels averaging 50 percent of the current threshold limit value (215 mg/m2) for 1-13 years (mean: 6 years). By comparison with a control group matched for age and socioeconomic status, no significant difference was observed in the urinary excretion of proteins. In rats, styrene was weakly nephrotoxic. No functional or morphological renal change could be disclosed in rats exposed to 565 mg of styrene/m3, 5 days/week for 13 weeks. The repeated i.p. injection of 1 g styrene/kg (1/5 of oral LD50) for 10 days induced only a slight tubular dysfunction as evidenced by a 5-fold increase in beta 2-microglobulinuria. Altogether, these epidemiological and experimental data suggest that the current threshold limit value for styrene (215 mg/m3) proposed by the American Conference of Governmental and Industrial Hygienists does not entail any risk of renal toxicity.

The response of the intestinal mucosa to Adriamycin (ADR) was studied in the duodenum, jejunum, and ileum of 25-day-old rats. A single injection of ADR resulted in decreases in mucosal DNA per centimeter of length and in sucrase activity, which were proportional to the doses given (2, 5, and 8 mg/kg). ADR at 2 mg/kg had no significant effect on body weight, gut length, epithelial structure, or mucosal protein content per unit length. The morphological modifications occurred mostly in the proximal intestine and consisted of villous atrophy and degenerative changes of villus and crypt cells. A single dose of 5 mg ADR/kg acutely affected the gut. At 48 and 96 h the changes were characterized by marked decreases in mucosal weight, DNA per centimeter, sucrase activity, and villous shortening. At 144 h, the ADR-treated intestine entered a highly proliferative state and showed increased villous height, mucosal weight, and DNA per centimeter. Although villous hyperplasia was observed at 144 and 192 h, the mucosal weight and DNA concentrations did not exceed the corresponding levels in the control. During the period of active epithelial proliferation, sucrase activity remained depressed. We conclude that in the growing rat: (a) the acute intestinal injury of ADR is short-lived, dose dependent, and predominates in the proximal small intestine; (b) the enteric mucosa reacts to cytotoxic injury by excessive proliferation of immature enterocytes; and (c) the hyperplastic response to ADR is confined to the mucosal epithelium.

Alinidine is a new bradycardic agent that interferes with ion channels and the if pacemaker current. To determine if alinidine had antiischemic effects unrelated to its bradycardic action, myocardial metabolism was studied during a pacing-stress test in 20 patients with coronary artery disease and angina pectoris, before and after intravenous infusion of alinidine (10 mg, n = 10; 50 mg, n = 10). When compared to the control pacing-stress test, the low dose of alinidine had no significant effect on aortic pressure, coronary sinus flow (-3%, NS), myocardial oxygen extraction, or myocardial lactate uptake. After the high dose of alinidine, aortic pressure and coronary sinus flow remained unchanged but the arteriocoronary sinus difference in oxygen content increased (12.2 +/- 1.3 to 12.7 +/- 1.4 ml/100 ml; p less than 0.0002) above the values observed during the control pacing-stress test, while both the chemical lactate extraction fraction (-19 +/- 30 to 15 +/- 21%; p less than 0.025) and the L-[1-14C]lactate extraction fraction increased. Accordingly, the net myocardial lactate uptake (corrected for production) had increased from 14 +/- 32 during the control pacing-stress test to 29 +/- 24 mumol/min during the pacing repeated after the high dose of alinidine (p less than 0.05). After the high dose of alinidine, the free fatty acid uptake also rose slightly (+23%; NS) and the alanine production was reduced in 7 of 10 patients (-3.6 +/- 1.7 to -1.4 +/- 0.6 mumol/min; NS).(ABSTRACT TRUNCATED AT 250 WORDS)

In order to determine whether pancreatic glucagon may influence growth of the small bowel mucosa and maturation of villous and crypt cell enzymes in orally fed rats, the hormone was administered daily to suckling pups from day 11 to day 14 (50 μg/day) and to weanling rats from day 12 to day 29 (100 μg/day) post partum. The control groups received, following the same schedule, an equal volume of 0.9% saline or of a glucagon diluent containing 0.2% phenol and 1.2% glycerine. In suckling pups treated with glucagon, sucrase and thymidine kinase activities were similar to those of the controls. During weaning, both glucagon- and diluent-treated rats grew slowlier (p < 0.05) than did saline controls. Histological examination of pancreatic -tissue sections from glucagon-treated rats showed partial or complete degranulation of the acinar cells. Compared to saline-treated controls, mucosal weight, protein and DNA per centimetre of gut remained unchanged in the duodenum, jejunum and ileum of glucagon-treated rats. However, these parameters were markedly depressed (p < 0.01) in animals treated with diluent. Prolonged treatment with glucagon during weaning had no effect on villus height, epithelial morphology and thymidine kinase activity but produced a decrease in both specific and total sucrase activity in the proximal intestine to levels about 50% (p < 0.01) of the saline controls. It is concluded that: (1) the administration of exogenous pancreatic glucagon does not induce early villous and crypt cell enzyme activity in the suckling rat; (2) at the given doses, the hormone does not impair the adaptation of the small intestine mucosa which occurs at weaning.

The nephrotoxic potential of S86451 (2′guanidyl, 2′deamino gentamicin C1) has been investigated in Sprague-Dawley rats at 10 and 25 mg/kg, in comparison with gentamicin at 4 and 10 mg/kg. The criteria were (i) the severity of the lysosomal phospholipidosis, as assessed by both biochemical and morphological investigations; (ii) the degree of tubular regeneration, a consequence of the aminoglycoside-induced focal necrosis measured by 3H-thymidine incorporation into kidney cortex DNA. S86451 was found at least 2–5 times less toxic than gentamicin. Thus, this compound should be a safer antibiotic than gentamicin in combating organisms with a similar sensitivity to either drug.

Kidney cortex DNA synthesis was studied in female rats treated with a low dose of gentamicin (10 mg/kg) up to 14 days. Synthesis was measured by incorporation of [3H]thymidine into DNA 1 h after intraperitoneal injection of the labeled precursor (200 muCi per animal). Gentamicin given in one injection per day resulted in a greater incorporation of [3H]thymidine into DNA after both 7 and 14 days of treatment as compared with control animals. When the daily dose was divided into three equal injections given at 8-h intervals, a statistically significant increase in thymidine incorporation was observed as early as 4 days after starting gentamicin administration. Excellent agreement was found between DNA specific radioactivity and kidney cortex nuclear labeling, as measured by histoautoradiography. The greatest amount of [3H]thymidine incorporation occurred within proximal tubular cells and interstitial cells. We conclude that a finite duration of gentamicin treatment at low dosage induces an increased DNA synthesis in vivo in rat kidney cortex. We suggest that this reaction results from cellular proliferation and could reflect a regenerative process after focal necrosis induced by gentamicin at low doses. The demonstrated early increase in DNA synthesis could be a useful tool to measure kidney cortex alterations caused by various aminoglycosides at low, therapeutic doses.

Ultrastructural alterations in the cortical, distal and collecting tubules have been examined in female Sprague-Dawley rats treated with various aminoglycosides in clinical use. Gentamicin, dibekacin (10 mg/kg X day), netilmicin, tobramycin (4 or 10 mg/kg X day) or amikacin (37.5 mg/kg X day) were administered intraperitoneally twice a day over different periods of time, extending from 4 to 14 days. The kidney cortex was examined after 4, 7, 10 or 14 days of aminoglycoside administration by light (semithin sections) and electron microscopy. After 7 or more days of treatment, lysosomes in collecting tubular cells (and to a lesser extent in distal tubular cells) contained concentric lamellar material (myeloid bodies), an ultrastructural alteration typical of drug-induced lysosomal phospholipidosis. Although this alteration appeared qualitatively similar to that observed in proximal tubular cells, it was less conspicuous and occurred later during treatment. In addition, distal tubular cells occasionally showed marked vacuolization and disruption of the basal cell architecture. The possible relationship between these alterations and the urine hypo-osmolality characteristic of aminoglycoside-induced renal dysfunction is discussed.