Percutaneous vertebroplasty is an efficient procedure to treat pain due to osteoporotic vertebral compression fractures. However, refracture of cemented vertebrae occurs occasionally after vertebroplasty. It is unclear whether such fractures are procedure-related or part of the natural course of osteoporosis. The effect of potentially important covariates on refracture risk in cemented vertebrae has not been evaluated previously. We retrospectively analyzed the incidence and possible causative mechanism of refracture in patients who had received only one vertebroplasty for a single level of vertebral compression fracture. We assessed the following covariates: age, sex, body weight, height, lumbar spine bone mineral density, treated vertebral level, pre-existing untreated vertebral compression fracture, and gas-containing vertebrae before treatment. Surgical variables, including surgical approach, cement injected, and anterior vertebral height restoration, were also analyzed. Antiosteoporotic treatment after surgery was recorded. Multiple logistic regression analysis was used to determine the relative risk of refractures of cemented vertebrae. Over all, 98 patients were evaluated with a mean follow-up of 26.9 ± 12.4 months (range, 7-55 months). We identified 62 refractures and the mean loss of anterior vertebral height was 13.3% (range 3.2-40.3%). The greater the anterior vertebral height obtained from vertebroplasty, the greater the risk of refracture occurring (P \ 0.01). Gas-containing vertebrae were also prone to refracture after the procedure (P = 0.01). Anti-osteoporotic treatment was of borderline significance between refractured and non-refractured vertebrae (P = 0.07). Only restoration of anterior vertebral height was positively associated with refracture during the follow-ups (P \ 0.01). In conclusion, refractures of cemented vertebrae after vertebroplasty occurred in 63% of osteoporotic patients. Significant anterior vertebral height restoration increases the risk of subsequent fracture in cemented vertebrae.

Complex biomolecules absorb in the mid-infrared ( ‫؍‬ 2-20 m), giving vibrational spectra associated with structure and function. We used Fourier transform infrared (FTIR) microspectroscopy to "fingerprint" locations along the length of human small and large intestinal crypts. Paraffinembedded slices of normal human gut were sectioned (10 m thick) and mounted to facilitate infrared (IR) spectral analyses. IR spectra were collected using globar (15 m ؋ 15 m aperture) FTIR microspectroscopy in reflection mode, synchrotron (<10 m ؋ 10 m aperture) FTIR microspectroscopy in transmission mode or near-field photothermal microspectroscopy. Dependent on the location of crypt interrogation, clear differences in spectral characteristics were noted. Epithelial-cell IR spectra were subjected to principal component analysis to determine whether wavenumber-absorbance relationships expressed as single points in "hyperspace" might on the basis of multivariate distance reveal biophysical differences along the length of gut crypts. Following spectroscopic analysis, plotted clusters and their loadings plots pointed toward symmetric ( s )PO 2 ؊ (1,080 cm ؊1 ) vibrations as a discriminating factor for the putative stem cell region; this proved to be a more robust marker than other phenotypic markers, such as ␤-catenin or CD133. This pattern was subsequently confirmed by image mapping and points to a novel approach of nondestructively identifying a tissue's stem cell location. s PO 2 ؊ , probably associated with DNA conformational alterations, might facilitate a means of identifying stem cells, which may have utility in other tissues where the location of stem cells is unclear.

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Lymphatic flow-positive but non-ICG enhanced LCVs, should also be considered as functional, thereby maximizing the number of functional LCVs for LVA.

Mesenchymal stem cells (MSCs) are usually cultured under normoxic conditions (21% oxygen). However, in vivo, the physiological "niches" for MSCs have a much lower oxygen tension. Because of their plasticity, stem cells are particularly sensitive to their environments, and oxygen tension is one developmentally important stimulus in stem cell biology and plays a role in the intricate balance between cellular proliferation and commitment towards differentiation. Therefore, we investigated here the effect of hypoxia (2% oxygen) on murine adipose tissue (AT) MSC proliferation and adipogenic differentiation. AT cells were obtained from the omental fat and AT-MSCs were selected for their ability to attach to the plastic dishes, and were grown under normoxic and hypoxic conditions. Prior exposure of MSCs to hypoxia led to a significant reduction of ex vivo expansion time, with significantly increased numbers of Sca-1(+) as well as Sca-1(+)/CD44(+)double-positive cells. Under low oxygen culture conditions, the AT-MSC number markedly increased and their adipogenic differentiation potential was reduced. Notably, the hypoxia-mediated inhibition of adipogenic differentiation was reversible: AT-MSCs pre-exposed to hypoxia when switched to normoxic conditions exhibited significantly higher adipogenic differentiation capacity compared to their pre-exposed normoxic-cultured counterparts. Accordingly, the expression of adipocyte-specific genes, peroxisome proliferator activated receptor gamma (Ppargamma), lipoprotein lipase (Lpl) and fatty acid binding protein 4 (Fabp4) were significantly enhanced in hypoxia pre-exposed AT-MSCs. In conclusion, pre-culturing MSCs under hypoxic culture conditions may represent a strategy to enhance MSC production, enrichment and adipogenic differentiation.

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Background: Lymphorrhea is probably the most appalling form of lymphedema and is difficult to treat. Intractable lymphorrhea is prone to infection because of skin breakdown. It is believed that supermicrosurgical lymphaticovenous anastomosis is unsuitable for treating such severe disease. Only a few lymphorrhea patients treated with lymphaticovenous anastomosis have been reported. Whether it can be used to treat lymphorrhea has remained inconclusive. Methods: From September of 2015 to June of 2018, 105 patients underwent supermicrosurgical lymphaticovenous anastomosis (n = 746) in the authors’ hospital. These patients are divided into the nonlymphorrhea group (three male and seven female patients) and the nonlymphedema group (lymphedema patients without lymphorrhea) (11 male and 84 female patients). Retrospective chart review with demographic data and intraoperative findings were recorded and analyzed. Post–lymphaticovenous anastomosis outcomes for lymphorrhea patients were also recorded. Results: No significant differences were found in patient age, sex, or affected limbs between these two groups. As for intraoperative findings, no differences were found in the percentage of indocyanine green–enhanced lymphatic vessels (52.7 ± 41.1 percent versus 67.3 ± 36.7 percent; p = 0.227) or the pathologic changes of lymphatic vessels based on the normal, ectasis, contraction, and sclerosis type classification (2.2 ± 1.0 versus 2.1 ± 1.0; p = 0.893) between the lymphorrhea and nonlymphorrhea groups, respectively. The average follow-up period was 14.5 months (range, 3 to 31 months). Five lymphorrhea patients (50 percent) showed complete recovery without relapse; significant lymphorrhea reduction was found in three patients (30 percent), and two patients showed minimal improvements (20 percent). Conclusion: With comparable functional lymphatic vessels identified in lymphorrhea patients, supermicrosurgical lymphaticovenous anastomosis is a viable option for lymphorrhea treatment, with satisfactory results. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, IV.

Chronic fatigue syndrome (CFS) is a complex disorder accompanied by unexplainable persistent fatigue, in which several etiological factors exist, such as viral infections. Using the National Health Insurance Research Database (NHIRD) of Taiwan, this study evaluated the association between herpes zoster (HZ) infection and the risk of CFS, and examined the possibility of patients developing postviral fatigue effects, including the possibility of developing other unexplainable chronic fatigue conditions. In this prospective cohort study using the NHIRD, we identified 9,205 patients with HZ infection [ICD-9 (International Classification of Disease, Ninth Revision), code 053] and 36,820 patients without HZ infection (non-HZ) from 2005 to 2007, and followed up to the end of 2010. The incidence rate of CFS was higher in the HZ cohort than in the non-HZ cohort (4.56 vs. 3.44 per 1,000 person-years), with an adjusted hazard ratio of 1.29 [95 % confidence interval (CI) = 1.09-1.53]. It was shown that the risk of CFS without comorbidity for each patient increased from 1.25- to 1.36-fold between the CFS and non-CFS cohorts; with long-term follow-up, the HZ cohort showed a significantly higher cumulative incidence rate of developing CFS than the non-HZ patients. We propose that patients with chronic fatigue might exist in a subset of patients that would be associated with HZ infection. The actual mechanism of development of CFS that is attributed to HZ infection remains unclear. The findings of this population cohort study provide pivotal evidence of postviral fatigue among patients with HZ infection.