Morphologic classification and innervation patterns of the pectineus muscle

The purpose of this study was to identify the frequency of pectineal hiatus and of pectineus innervations, including femoral, obturator, and/or accessory obturator nerves. Also, this study sought to detailed intramuscular nervous distributions, with a particular focus on the relationship of nerves in multi-innervated pectineus. One hundred (49 right and 51 left) thighs from 52 cadavers (25 men and 27 women) were dissected. The morphology and innervations of the pectineus were investigated. Modified Sihler’s whole-mount nerve-staining method was employed for visualization of the intramuscular nerve-distribution patterns of the pectineus. Variation of the pectineus forming a hiatus was identified in 18% of the specimens. The femoral innervations to the pectineus were identified in all specimens. Additional innervation either by the obturator or the accessory obturator branch to the pectineus was identified in 10% or 2% of specimens, respectively. No case of triple innervation to the pectineus was observed. In cases of dually innervated pectineus, two nerves formed a communication system inside the muscle. Among the three nerves supplying the pectineus, the femoral nerve branched more than the other two nerves and covered the greatest area in the muscle. The pectineal hiatus appears to be a common variation. The femoral nerve branch in a dually innervated pectineus is the dominant nerve component that supplies the muscle when considering frequency, branching pattern, and area, even though cooperation between two nerve components is implied. This study serves to advance the existing anatomical knowledge about the pectineus muscle, which is of clinical value.

     

Automated Computational Detection of Interstitial Fibrosis,Tubular Atrophy,and Glomerulosclerosis

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Relation Between Tumor Size and Lymph Node Metastasis According to Subtypes of Breast Cancer

PurposeTumor size and lymph node metastasis are important factors that contribute to the progression of breast cancer. We aimed to analyze the relationship between tumor size and lymph node metastasis molecular subtype and examine the effects of nodal metastasis on overall survival (OS).MethodsWe retrospectively reviewed the data of 16,552 patients who underwent breast surgery in Samsung Medical Center between 2000 and 2015. Information on tumor size (largest diameter of the invasive component), number of positive lymph nodes, and molecular subtype were obtained. We constructed a linear regression model to evaluate the relationship between tumor size and lymph node metastasis. To determine the effect of nodal metastasis on OS, we performed a Cox proportional regression analysis with Np/T (number of metastatic lymph nodes [n]/tumor size [cm]).ResultsThis study included 12,007 patients with a median follow-up of 62 months. The linear regression coefficients were 1.043 for luminal A, 1.024 for luminal B, 0.656 for HER2, and 0.435 for triple-negative breast cancer (TNBC) subtypes. No significant difference was observed in the coefficients between the luminal A and B subtypes (p = 0.797), while all other coefficients showed significant difference. After adjusting for other risk factors, the hazard ratio (HR) of Np/T for each subtype was significant for OS: luminal A (HR, 1.134; 95% confidence interval [CI], 1.097–1.171; p < 0.001), luminal B (HR, 1.049; 95% CI, 1.013–1.086; p = 0.007), HER2 (HR, 1.069; 95% CI, 1.014–1.126; p = 0.013), and TNBC (HR, 1.038; 95% CI, 1.01–1.067; p = 0.008).ConclusionThe incidence of lymph node metastasis differed according to molecular subtype. Luminal types have higher incidence of nodal metastasis than HER2 and TNBC. The HR of Np/T was highest in luminal A subtypes and lowest in TNBC subtypes.     

Pancreatic stellate cells in the islets as a novel target to preserve the pancreatic β‐cell mass and function

There are numerous lines of clinical evidence that inhibition of the renin–angiotensin system (RAS) can prevent and delay the development of diabetes. Also, the role of RAS in the pathogenesis of diabetes, including insulin resistance and β‐cell dysfunction, has been extensively investigated. Nevertheless, this role had not yet been fully shown. A variety of possible protective mechanisms for RAS blockers in the regulation of glucose homeostasis have been suggested. However, the direct effect on pancreatic islet fibrosis has only recently been spotlighted. Various degrees of islet fibrosis are often observed in the islets of patients with type 2 diabetes mellitus, which can be associated with a decrease in β‐cell mass and function in these patients. Pancreatic stellate cells are thought to be deeply involved in this islet fibrosis. In this process, the activation of RAS in islets is shown to transform quiescent pancreatic stellate cells into the activated form, stimulates their proliferation and consequently leads to islet fibrotic destruction. In this article, we introduce existing clinical and experimental evidence for diabetes prevention through inhibition of RAS, and review the responsible local RAS signaling pathways in pancreatic stellate cells. Finally, we propose possible targets for the prevention of islet fibrosis.     

Short or Long Sleep Duration and CKD: A Mendelian Randomization Study

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