Larynx preservation surgery in pyriform sinus cancer

As a general rule, surgery, whenever possible followed by irradiation, is considered to be a standard treatment for pyriform sinus cancer. In early primary lesions, many different approaches have been tried for larynx preservation. From 1990-1997, 7 patients with pyriform sinus carcinoma without the involvement of pyriform sinus apex were treated with partial laryngopharyngectomy at the Asan Medical Center. Three patients were T1 stage and four were T2. All patients had nodal metastases and were treated with neck dissection and postoperative radiotherapy. Follow-up period was 1-8 years. One regional recurrence and one distant metastasis occurred; however, there was no recurrence at the primary site. The voices of all the patients were saved. The most uncomfortable postoperative symptom was mild aspiration. From these results, we can conclude that partial laryngopharyngectomy with neck dissection might be the favorable treatment modality for selected cases of pyriform sinus cancer.     

Malignant transformation of nevus sebaceous to basal-cell carcinoma: Case series,literature review,and management algorithm

Nevus sebaceous (NS) is a common congenital hamartoma of the skin composed predominantly of sebaceous glands. Although most NS are benign skin tumors, malignant transformations have been reported. There is still controversy about the lifetime risk of malignant degeneration and precise surgical criteria. This study reports cases of malignant degeneration and suggests a surgical treatment algorithm. The medical records of patients with basal-cell carcinoma (BCC) arising from NS between January 2001 and January 2021 were retrospectively reviewed. Patient demographics including lesion location, and tumor size were investigated. The symptoms, histological findings before and after excision, complications, and recurrence during 2-year follow-up periods were investigated. Ten patients were identified with BCC arising from NS lesions. All patients were female and the mean age was 52.11 years. All patients complained of sudden morphological changes, the most common type being rapid color changes. Two cases had histological findings that showed a miss-match between punch biopsy and excisional biopsy results. No recurrence was detected 2 years after surgeries in any patients. Cases after third stage, especially in over 40 years who report morphologic changes, should undergo total surgical excision as the first approach, with strong suspicion of malignant degeneration.     

The Alleviation of Gut Microbiota-Induced Depression and Colitis in Mice by Anti-Inflammatory Probiotics NK151, NK173, and NK175

Gut microbiota dysbiosis is strongly associated with psychiatric disorders and inflammatory bowel disease (IBD). Herein, we examined whether the fecal microbiota of IBD patients with depression (IBDD) and their gut microbiota culture (iGm) could cause depression and colitis in mice and anti-inflammatory probiotics could mitigate depression in iGm-transplanted or immobilization stress (IS)-exposed mice. Fecal microbiota transplantation (FMT) from IBDD patients, which exhibited Enterobacteriaceae-rich gut microbiota, and its gut microbiota culture (iGm) increased depression-like behaviors in mice. Their treatments heightened the blood lipopolysaccharide (LPS) level and colonic IL-1β and IL-6 expression. However, FMT from healthy volunteers or sulfasalazine treatment alleviated cGm-induced depressive-like behaviors and hippocampal and colonic inflammation in mice. Moreover, oral administration of Lactobacillus plantarum NK151, Bifidobacterium longum NK173, and Bifidobacterium bifidum NK175, which inhibited LPS-induced IL-6 expression in macrophages, alleviated cGm-induced depression-like behaviors, hippocampal NF-κB⁺Iba1⁺ cell numbers and IL-1β and IL-6 expression, blood LPS, IL-6, and creatinine levels, and colonic NF-κB⁺CD11c⁺ number and IL-1β and IL-6 expression in mice. Treatment with NK151, NK173, or NK175 mitigated immobilization stress (IS)-induced depressive-like behaviors, neuroinflammation, and gut inflammation in mice. NK151, NK173, or NK175 also decreased IS-induced blood LPS, IL-6, and creatinine levels. The transplantation of Enterobacteriaceae-rich gut microbiota can cause depression and colitis, as IS exposure, and anti-inflammatory NK151, NK173, and NK175, may alleviate stress-induced fatigue, depression, and colitis by regulating the expression of proinflammatory and anti-inflammatory cytokines through the suppression of gut bacterial LPS.     

维药胡桐泪的多糖含量测定及其糖组成分析

目的:测定市场上实际流通的商品胡桐泪药材中多糖的含量并对其单糖组成进行分析,以多糖为指标评价药材质量。方法:采用苯酚-硫酸法对总多糖进行含量测定;应用核磁共振氢谱(1H-NMR)分析单糖组成;运用高效凝胶渗透色谱(HPGPC)测定总多糖的分子量分布。结果:以葡萄糖计,4批新式胡桐泪总多糖含量平均值为(7.36±1.74)%,6批老式胡桐泪总多糖含量平均值为(1.53±0.99)%;新式与老式胡桐泪总多糖的单糖组成相似,主要由阿拉伯糖和半乳糖组成,还含有木糖、甘露糖、鼠李糖等,部分样品尚含有较高含量的葡萄糖;新旧类型样品总多糖在分子量分布上存在较大差异。结论:新式胡桐泪的总多糖含量平均值较老式高,以多糖含量为评价指标时,新式样品总体质量较老式更好;应用核磁共振氢谱可以快速、准确地鉴定单糖组成。     

Brief Report: Adenosine A2A receptor blockade prevents cisplatin-induced impairments in neurogenesis and cognitive function

Chemotherapy-induced cognitive impairment (CICI) has emerged as a significant medical problem without therapeutic options. Using the platinum-based chemotherapy cisplatin to model CICI, we revealed robust elevations in the adenosine A_2A receptor (A_2AR) and its downstream effectors, cAMP and CREB, by cisplatin in the adult mouse hippocampus, a critical brain structure for learning and memory. Notably, A_2AR inhibition by the Food and Drug Administration–approved A_2AR antagonist KW-6002 prevented cisplatin-induced impairments in neural progenitor proliferation and dendrite morphogenesis of adult-born neurons, while improving memory and anxiety-like behavior, without affecting tumor growth or cisplatin’s antitumor activity. Collectively, our study identifies A_2AR signaling as a key pathway that can be therapeutically targeted to prevent cisplatin-induced cognitive impairments.     

Full-Endoscopic versus Minimally Invasive Lumbar Interbody Fusion for Lumbar Degenerative Diseases : A Systematic Review and Meta-Analysis

ObjectiveAlthough full-endoscopic lumbar interbody fusion (Endo-LIF) has been tried as the latest alternative technique to minimally invasive transforaminal lumbar interobody fusion (MIS-TLIF) since mid-2010, the evidence is still lacking. We compared the clinical outcome and safety of Endo-LIF to MIS-TLIF for lumbar degenerative disease. MethodsWe systematically searched electronic databases, including PubMed, EMBASE, and Cochrane Library to find literature comparing Endo-LIF to MIS-TLIF. The results retrieved were last updated on December 11, 2020. The perioperative outcome included the operation time, blood loss, complication, and hospital stay. The clinical outcomes included Visual analog scale (VAS) of low back pain and leg pain and Oswestry disability index (ODI), and the radiological outcome included pseudoarthosis rate with 12-month minimum follow-up. ResultsFour retrospective observational studies and one prospective observational study comprising 423 patients (183 Endo-LIF and 241 MIS-TLIF) were included, and the pooled data analysis revealed low heterogeneity between studies in our review. Baseline characteristics including age and sex were not different between the two groups. Operation time was significantly longer in Endo-LIF (mean difference [MD], 23.220 minutes; 95% confidence interval [CI], 10.669–35.771; p=0.001). However, Endo-LIF resulted in less perioperative blood loss (MD, -144.710 mL; 95% CI, 247.941–41.478; p=0.023). Although VAS back pain at final (MD, -0.120; p=0.586), leg pain within 2 weeks (MD, 0.005; p=0.293), VAS leg pain at final (MD, 0.099; p=0.099), ODI at final (MD, 0.141; p=0.093) were not different, VAS back pain within 2 weeks was more favorable in the Endo-LIF (MD, -1.538; 95% CI, -2.044 to -1.032; p<0.001). On the other hand, no statistically significant group difference in complication rate (relative risk [RR], 0.709; p=0.774), hospital stay (MD, -2.399; p=0.151), and pseudoarthrosis rate (RR, 1.284; p=0.736) were found. ConclusionRelative to MIS-TLIF, immediate outcomes were favorable in Endo-LIF in terms of blood loss and immediate VAS back pain, although complication rate, mid-term clinical outcomes, and fusion rate were not different. However, the challenges for Endo-LIF include longer operation time which means a difficult learning curve and limited surgical indication which means patient selection bias. Larger-scale, well-designed study with long-term follow-up and randomized controlled trials are needed to confirm and update the results of this systematic review.     

β-Sitosterol Attenuates Dexamethasone-Induced Muscle Atrophy via Regulating FoxO1-Dependent Signaling in C2C12 Cell and Mice Model

Sarcopenia refers to a decline in muscle mass and strength with age, causing significant impairment in the ability to carry out normal daily functions and increased risk of falls and fractures, eventually leading to loss of independence. Maintaining protein homeostasis is an important factor in preventing muscle loss, and the decrease in muscle mass is caused by an imbalance between anabolism and catabolism of muscle proteins. Although β-sitosterol has various effects such as anti-inflammatory, protective effect against nonalcoholic fatty liver disease (NAFLD), antioxidant, and antidiabetic activity, the mechanism of β-sitosterol effect on the catabolic pathway was not well known. β-sitosterol was assessed in vitro and in vivo using a dexamethasone-induced muscle atrophy mice model and C2C12 myoblasts. β-sitosterol protected mice from dexamethasone-induced muscle mass loss. The thickness of gastrocnemius muscle myofibers was increased in dexamethasone with the β-sitosterol treatment group (DS). Grip strength and creatine kinase (CK) activity were also recovered when β-sitosterol was treated. The muscle loss inhibitory efficacy of β-sitosterol in dexamethasone-induced muscle atrophy in C2C12 myotube was also verified in C2C12 myoblast. β-sitosterol also recovered the width of myotubes. The protein expression of muscle atrophy F-box (MAFbx) was increased in dexamethasone-treated animal models and C2C12 myoblast, but it was reduced when β-sitosterol was treated. MuRF1 also showed similar results to MAFbx in the mRNA level of C2C12 myotubes. In addition, in the gastrocnemius and tibialis anterior muscles of mouse models, Forkhead Box O1 (FoxO1) protein was increased in the dexamethasone-treated group (Dexa) compared with the control group and reduced in the DS group. Therefore, β-sitosterol would be a potential treatment agent for aging sarcopenia.     

Enchondral cartilage rests collagen-induced autoimmunity: a possible pathogenetic mechanism of otosclerosis

Collagen autoimmunity has been suggested as one etiologic mechanism to otosclerosis. Although substantial studies relating this disease to collagen autoimmunity have been reported, a basic understanding of the pathogenic mechanism involved is lacking. Some otosclerosis patients have a high level of antibody to type II collagen. In addition, complement and antibody were deposited in the stapes from otosclerosis patients. Furthermore, the otic capsule and stapes have been found to contain type II collagen by immunohistologic studies and biochemical analysis. Otospongiosis-like lesions have also been produced in rats by immunizing them with type II collagen. This finding led us to postulate a hypothesis of an autoimmunity to type II collagen as an etiopathogenesis of this illness. Our initial hypothesis has been updated to incorporate new findings in the field of cell biology. The role of interleukin 1, osteoclasts, osteoblasts, bone resorption, and other factors such as minor collagens, calcitonin, vitamin D, parathyroid hormone, collagenase, and prostaglandins are incorporated in this updated hypothesis.