A new posture measurement method for measuring intrinsic standing posture

Aims: Although body posture in relation to the dental condition has been of great interest in the dental profession, rumination bias has been a substantial obstacle to achieving a reliable objective evaluation of the intrinsic body posture. The aim of this study was to establish a posture control protocol that would minimize the effect of bias.

Methodology: Fifteen healthy male volunteers (23–33 years of age) participated in this study. The posture movement was recorded for 10 seconds by a three-dimensional motion capture system. The experiment was performed on four different days.

Results: The posture was most stable at 4–5 seconds after the start of the front bulb gaze (the mean coefficient of variation ranged from 0·1 to 44·1). The intraclass correlation coefficients for four days were 0·871–0·975 (P≤0·001).

Conclusions: It was concluded that the use of this measurement method helped in producing a reliable intrinsic standing posture where unbiased evaluation of the effect of any intervention on the body posture is researched.     

Neonatal estrogen treatment with β-estradiol 17-cypionate induces in post-pubertal mice inflammation in the ductuli efferentes,epididymis, and vas deferens,but not in the testis,provoking obstructive azoospermia

Neonatal estrogen treatment (NET) induces morphological changes in male reproductive organs. NET with β-estradiol 17-cypionate is reported to induce inflammation with stromal-epithelial abnormalities in the prostate and seminal vesicles in post-pubertal mice. The aim of this study was to investigate the histopathology of the testis, ductuli efferentes, epididymis, and vas deferens in mice after NET with β-estradiol 17-cypionate. No morphological changes in these organs were observed until 4 weeks after NET. However, some inflammatory cells were found in epididymis and vas deferens 6 weeks after NET. Eight weeks after NET, inflammatory cells spread to the ductuli efferentes and inflammation was severe from 6 to 12 weeks after NET. Inflammatory cells were never seen in the whole testis, but cystic dilatation of the rete testes with spermatogenic disturbance was found around the mediastinum testis. Many inflammatory cells emigrated into the lumen of the epididymis, resulting in complete absence of spermatozoa in the vas deferens. Most of the inflammatory cells penetrating into the epithelial layers of epididymal ducts were neutrophils. These results indicate that in post-pubertal mice, NET with β-estradiol 17-cypionate induces inflammation in the ductuli efferentes, epididymis, and vas deferens, but not in the testis, provoking obstructive azoospermia.     

Hepatitis B virus X stimulates redox signaling through activation of ataxia telangiectasia mutated kinase

Hepatitis B virus X (HBX) protein plays a crucial role in carcinogenesis, but its mechanism is unclear. The involvement of ataxia telangiectasia mutated (ATM) kinase in the enhanced redox system was investigated by examining the phosphorylation level of ATM in HBX gene-transfected cells and in transgenic mice following redox system manipulation by treatment with hydrogen peroxide (H₂O₂) or antioxidant. Western blotting and immunostaining showed that phospho-ATM was significantly increased by HBX both in vitro (3.2-fold; p<0.05) and in vivo (4-fold; p<0.05), and this effect was abrogated by antioxidant treatment. The level of PKC-δ in HBX-expressing cells was increased 3.5-fold compared to controls. Nuclear localized NF-E2-related factor 2 (Nrf2) was increased in HBX-expressing cells exposed to H₂O₂, but remained at lower levels after the treatment with rottlerin, KU55933, or caffeine. The levels of anti-oxidant molecules were increased in HBX expressing cells and in transgenic mice, indicating that HBX stimulates the Nrf2-mediated redox system. The levels of intracellular reactive oxygen species (ROS) were significantly increased in HBX-expressing cells treated with hydrogen peroxide in the presence of ATM inhibitor KU55933 or caffeine. Treatment of HBX-expressing cells with KU55933 or caffeine before the exposure to H₂O₂ increased the ratio of cell apoptosis to 33 ± 4% (p<0.05) and 22 ± 4% (p<0.05), respectively. Collectively, HBX stimulates the ATM-mediated PKC-δ/Nrf2 pathway, and maintains the enhanced activity of the redox system. Therefore, manipulating ATM kinase activity might be a useful strategy for treating HBX-induced carcinogenesis.     

Granulocyte colony-stimulating factor-producing undifferentiated carcinoma of the colon mimicking a pulmonary giant cell carcinoma: a case showing overexpression of CD44 along with highly proliferating nestin-positive tumor vessels

Granulocyte colony-stimulating factor (G-CSF)-producing tumors are known for their aggressive behavior. Only four cases of G-CSF-producing colorectal carcinoma have been previously reported. Herein, we present a case of an undifferentiated carcinoma of the descending colon showing G-CSF production and giant cell carcinoma morphology in a 93-year-old woman. A tumor with a diameter of 80 mm was identified in the descending colon via computed tomography. Descending colectomy was performed involving the abdominal wall where tumor invasion was observed. The white blood cell count, which was elevated before resection, decreased to normal levels after intervention. However, local recurrence at the resected site was detected 39 days after surgery. Upon recurrence, increased white blood cell counts and serum G-CSF were seen. The patient died because of respiratory failure 98 days after colectomy. By using immunohistochemistry, G-CSF expression was detected in tumor cells in the resected specimen, along with overexpression of CD44 and highly proliferating nestin-positive tumor vessels. The poor clinical outcome of this patient is consistent with previous reports that the expression of these three molecules predict poor prognosis. While G-CSF can be a therapeutic target considering its auto/paracrine function to induce tumor growth via the G-CSF receptor, CD44 and nestin may also be possible candidate therapeutic targets. Further studies are required to assess the efficacy of treatments targeting these three molecules.     

Short- and long-term clinical effects of primary directional coronary atherectomy for acute myocardial infarction

We performed primary directional coronary atherectomy (DCA) without antecedent thrombolytic therapy in 21 of 67 patients with acute myocardial infarction within 24 hr of onset between June 1993–March 1994. Reperfusion with primary DCA was successful in 18 patients (85.7%, group D). Results were compared with those of primary balloon angioplasty patients treated between June 1992–May 1993 (group P). Minimum lumen diameter (MLD) values both immediately after reperfusion and in predischarge angiograms were significantly larger in group D than in group P, but were similar in late follow-up angiograms. Although a larger MLD in group D than in group P contributed to the prevention of reocclusion of the coronary artery before discharge in DCA patients, a high rate of restenosis at late follow-up canceled the beneficial effects of primary DCA. © 1996 Wiley-Liss, Inc.     

Prediction of early progression of metastatic renal cell carcinoma treated with first-line tyrosine kinase inhibitor

Background:There are various alternative first-line therapeutic options besides tyrosine kinase inhibitors (TKIs) for metastatic renal cell carcinoma (mRCC). To inform therapeutic decision-making for such patients, this study aimed to identify predictive factors for resistance to TKI.Materials and methods:A total of 239 cases of mRCC patients who received first-line TKI therapy were retrospectively studied. Patients with a radiologic diagnosis of progressive disease within 3 months after initiating therapy were classified as primary refractory cases; the others were classified as non-primary refractory cases. The association between primary refractory cases and age, gender, pathology findings, serum c-reactive protein (CRP) level, metastatic organ status, and 6 parameters defined by the International Metastatic Renal Cell Carcinoma Database Consortium were analyzed.Results:Of 239 cases, 32 (13.3%) received a radiologic diagnosis of progressive disease within 3 months after initiating therapy. The rates of sarcomatoid differentiation, hypercalcemia, a serum CRP level of 0.3 mg/dL or higher, presence of liver metastasis, anemia, and time from diagnosis to treatment interval of less than a year were significantly higher in the primary refractory group. Multivariate analysis showed that sarcomatoid differentiation, hypercalcemia, a serum CRP level of 0.3 mg/dL or higher, and liver metastasis were independently associated with primary refractory disease. A risk-stratified model based upon the number of patients with these factors indicated rates of primary refractory disease of 4.0%, 10.1%, and 45.0% for patients with 0, 1, and 2 or more factors, respectively.Conclusions:Sarcomatoid differentiation, hypercalcemia, an elevated serum CRP level, and presence of liver metastasis were associated with primary refractory disease in mRCC patients receiving first-line TKI therapy. These results provide clinicians with useful information when selecting a first-line therapeutic option for mRCC patients.     

Paraneoplastic Opsoclonus-myoclonus Syndrome with Anti-Hu and Anti-SOX-1 Antibodies after Immune-checkpoint Inhibitor Treatment Combined with Chemotherapy in a Patient with Small-cell Lung Cancer

A 69-year-old man with advanced small-cell lung cancer achieved partial remission after 3 courses of immunochemotherapy that included atezolizumab. Ten days after the last treatment, he developed paraneoplastic opsoclonus-myoclonus syndrome and required mechanical ventilation. Serology testing detected anti-Hu and anti-SOX-1 antibodies. Despite steroid pulse therapy, various anticonvulsants, continuous intravenous sedation, and a fourth course of chemotherapy without atezolizumab, his condition failed to improve. Paraneoplastic opsoclonus-myoclonus syndrome with autoantibodies after immune-checkpoint inhibitor treatment has not been reported previously. Although a causal relationship between immune-checkpoint inhibitors and paraneoplastic syndromes has been suggested, the mechanism remains unknown.