Surveillance study of the prevalence, species distribution, antifungal susceptibility, risk factors and mortality of invasive candidiasis in a tertiary teaching hospital in Southwest China.

BACKGROUND: Invasive candidiasis (IC) is the most common invasive fungal infection. The epidemiology of IC in hospitalized patients has been widely investigated in many metropolitan cities; however, little information from medium and small cities is known. METHODS: A 5-year retrospective study was carried out to analyze the prevalence, species distribution, antifungal susceptibility, risk factors and mortality of inpatients with invasive Candida infection in a regional tertiary teaching hospital in Southwest China. RESULTS: A total of 243 inpatients with invasive Candida infection during the five-year study period were identified, with a mean annual incidence of 0.41 cases per 1000 admissions and a 30-day mortality rate of 12.3%. The species distributions of Candida albicans, Candida glabrata, Candida tropicalis, Candida krusei, Candida parapsilosis and other Candida species was 45.3, 30.0, 15.2, 4.9, 2.1 and 2.5%, respectively. The total resistance rates of fluconazole (FCA), itraconazole (ITR) and voriconazole (VRC) were 18.6, 23.1 and 18.5%, respectively. Respiratory dysfunction, pulmonary infection, cardiovascular disease, chronic/acute renal failure, mechanical ventilation, abdominal surgery, intensive care in adults, septic shock and IC due to C. albicans were associated with 30-day mortality (P < 0.05) according to the univariate analyses. Respiratory dysfunction [odds ratio (OR), 9.80; 95% confidence interval (CI), 3.24-29.63; P < 0.001] and IC due to C. albicans (OR, 3.35; 95% CI, 1.13-9.92; P = 0.029) were the independent predictors of 30-day mortality. CONCLUSIONS: This report shows that the incidence and mortality rates are lower and that the resistance rates to azoles are higher in medium and small cities than in large cities and that the species distributions and risk factors in medium and small cities are different from those in large cities in China. It is necessary to conduct epidemiological surveillance in medium and small cities to provide reference data for the surveillance of inpatients with IC infections.

Unilateral vertebral artery injury in a patient with displaced upper cervical spine fractures: the treatment for one case of vertebral artery embolism.

PURPOSE: To report a novel treatment method for vertebral artery injury. Vertebral artery injuries may be caused during trauma by fracture and excessive motion with subluxation from C2 to C6 in spite of vertebral artery deeply seated and normally well protected inside the transverse foramen. Optimal medical management of the occluded vertebral artery has yet to be determined. METHODS: We report on a severely displaced C2-C3 fracture that was found to have a vertebral artery injury. Medical records and imaging were reviewed. RESULTS: A 50-year-old lady was hit by steel tube without loss of consciousness, but complaining of severe cervical and bilateral periscapular pain. Physical examination identified a neurologically intact patient with frontotemporal ecchymosis and posterior cervical tenderness. MRA and DSA showed an occluded left vertebral artery. After 3 days of observation, the patient showed no symptoms of brain ischemia or abnormal sensation and motor at four limbs. To ensure safety, we took the left vertebral artery embolism at the C2 and C5 levels before operation. CONCLUSIONS: To our knowledge, this is the first report of a displaced C2-C3 fracture in which transcatheter unilateral VAI embolization was used to prevent VAI bleeding during operation.

Serum Isthmin-1 is negatively correlated with HDL-C in type 2 diabetes mellitus.

BACKGROUND: Isthmin-1 (Ism-1) is a newly identified insulin-like adipokine that increases glucose uptake by adipocytes and inhibits hepatic lipid synthesis. Recent studies have shown that Ism-1 can improve the metabolic disorders associated with type 2 diabetes mellitus (T2DM) and improve lipid metabolism. The classic function of high-density lipoprotein cholesterol (HDL-C) is to transport cholesterol from extra-hepatic tissues to the liver for metabolism. In contrast, disorders of lipid metabolism and inflammation are the leading causes of atherosclerosis (As). Atherosclerosis often manifests as loss of elasticity, lipid accumulation, fibrous tissue proliferation and calcium deposits in the affected arteries, eventually forming plaques. AIM: To illustrate the correlation between HDL-C and Ism-1 in T2DM, and the relationship between lipoprotein cholesterol and carotid plaque. METHODS: A total of 128 patients with T2DM were enrolled in the study and basic information was collected. HDL-C levels were measured chemically. Serum Ism-1 levels were measured using an enzyme-linked immunosorbent assay (ELISA). Linear regression analysis was used to assess the correlation between serum Ism-1 levels and HDL-C in patients with T2DM. Basic information was again collected from 226 patients with T2DM. Independent sample t-tests were performed to explore the relationship between carotid plaque formation and lipids. RESULTS: HDL-C was divided into four groups according to quartiles and there was a between-group difference in Ism-1 (p = 0.040). Multivariable linear regression showed a negative association between Ism-1 and HDL-C in T2DM (ß = -0.235, p < 0.001), even after adjusting for related factors (ß = -0.165, p = 0.009). Low-density lipoprotein cholesterol (LDL-C) and HDL-C showed significant differences between the carotid plaque group and the non-carotid plaque group (pLDL-C = 0.007, pHDL-C = 0.003). CONCLUSION: Serum Ism-1 and HDL-C are negatively correlated in T2DM. LDL-C is significantly higher in carotid plaque group than non-carotid plaque group, while HDL-C is significantly lower than in the non-carotid plaque group.

The causal relationship between metabolic factors, drinking, smoking and intrahepatic cholangiocarcinoma: a Mendelian randomization study.

Background: Intrahepatic cholangiocarcinoma (iCCA) is the second most common primary liver cancer. While multiple risk factors for iCCA have been established, metabolic diseases (obesity, diabetes, NAFLD, dyslipidemia, and hypertension) and other risk factors, including smoking and drinking, are still controversial due to their potential confounders. Here, Mendelian randomization (MR) analysis was performed to identify the causal relationship between them. Method: In this study, we obtained GWAS data related to exposures from corresponding large genome-wide association studies. Summary-level statistical data for iCCA were obtained from the UK Biobank (UKB). We performed a univariable MR analysis to identify whether genetic evidence of exposure was significantly associated with iCCA risk. A multivariable MR analysis was conducted to estimate the independent effects of exposures on iCCA. Results: Univariable and multivariable MR analysis based on the large GWAS data indicated that there is little evidence to support the genetic role of metabolic factors, smoking, drinking, and NAFLD in iCCA development (P >0.05). In contrast to most current studies, their impact on iCCA development, if any, might be smaller than we thought. The previous positive results might be due to the comorbidities between diseases and potentially unavoidable confounding factors. Conclusion: In this MR study, we found no strong evidence to support causal associations between metabolic factors, NAFLD, smoking, drinking, and iCCA risk.

Neuron-Derived Exosomes Promote the Recovery of Spinal Cord Injury by Modulating Nerve Cells in the Cellular Microenvironment of the Lesion Area.

During spinal cord injury (SCI), the homeostasis of the cellular microenvironment in the injured area is seriously disrupted, which makes it extremely difficult for injured neurons with regenerative ability to repair, emphasizing the importance of restoring the cellular microenvironment at the injury site. Neurons interact closely with other nerve cells in the central nervous system (CNS) and regulate these cells. However, the specific mechanisms by which neurons modulate the cellular microenvironment remain unclear. Exosomes were isolated from the primary neurons, and their effects on astrocytes, microglia, oligodendrocyte progenitor cells (OPCs), neurons, and neural stem cells were investigated by quantifying the expression of related proteins and mRNA. A mouse SCI model was established, and neuron-derived exosomes were injected into the mice by the caudal vein to observe the recovery of motor function in mice and the changes in the nerve cells in the lesion area. Neuron-derived exosomes could reverse the activation of microglia and astrocytes and promote the maturation of OPCs in vivo and in vitro. In addition, neuron-derived exosomes promoted neurite outgrowth of neurons and the differentiation of neural stem cells into neurons. Moreover, our experiments showed that neuron-derived exosomes enhanced motor function recovery and nerve regeneration in mice with SCI. Our findings highlight that neuron-derived exosomes could promote the repair of the injured spinal cord by regulating the cellular microenvironment of neurons and could be a promising treatment for spinal cord injury.

Spinal cord injury causes more damage to fracture healing of later phase than ovariectomy in young mice.

The purpose of this study was to compare the effects of spinal cord injury (SCI) and ovariectomy (OVX) on femoral fracture healing of later phase in young mice. Sixty young female C57 mice were randomized into three groups: SCI, OVX, and age-matched intact control. The femoral fracture was generated at 3 weeks after SCI or OVX. At 1 month after fracture, the femoral fracture area was evaluated through the healing status using radiograph; bone mineral density using dual X-ray absorptometry; callus formation and mineralization and neovascularization in callus using micro-computed tomography; biomechanical analysis using testing machine; and histology analysis by staining with hematoxylin-eosin stain. SCI mice showed lower bone mineral density in the femoral callus as compared with OVX mice. Callus geometric microstructural parameters of the femora in SCI mice were significantly lower than OVX mice. SCI induced significant changes of biomechanical parameters in the femoral fracture healing area. The callus formation and callus neovascularization in SCI mice were significantly lower than in OVX mice. SCI induces more deterioration of fracture healing in the femoral diaphysis than OVX.

Difference in intraosseous blood vessel volume and number in osteoporotic model mice induced by spinal cord injury and sciatic nerve resection.

In the present study, we examined intraosseous blood vessel parameters of the tibial metaphysis in mice using microcomputed tomography (µCT) to investigate the relationship between post-nerve-injury osteoporosis and local intraosseous blood vessel volume and number. Mice were randomly divided into groups receiving spinal cord injury (SCI), sciatic nerve resection group (NX), or intact controls (30 mice/group). Four weeks after surgery, mice were perfused with silicone and the distribution of intraosseous blood vessels analyzed by µCT. The bone density, µCT microstructure, biomechanical properties, and the immunohistochemical and biochemical indicators of angiogenesis were also measured. The SCI group showed significantly reduced tibial metaphysis bone density, µCT bone microstructure, tibial biomechanical properties, indicators of angiogenesis, and intraosseous blood vessel parameters compared to the NX group. Furthermore, the spinal cord-injured mice exhibited significantly decreased intraosseous blood vessel volume and number during the development of osteoporosis. In conclusion, these data suggest that decreased intraosseous blood vessel volume and number may play an important role in the development of post-nerve-injury osteoporosis.

[Correlation of large artery stiffness and coronary flow velocity reserve].

OBJECTIVE: Coronary flow velocity reserve (CFVR) is an important indicator of coronary endothelial functions and microcirculation. Pulse wave velocity (PWV) reflects the degree of aortic sclerosis and it is an independent predictor of cardiovascular events. The present study was designed to evaluate the correlation of large artery stiffness and CFVR. METHODS: A total of 101 consecutive subjects were enrolled to measure the brachial-ankle pulse wave velocity (baPWV). According to the presence or absence of higher baPWV (> 1400 cm/s), they were divided into 2 groups. Transthoracic echocardiography was employed to measure coronary flow velocity in coronary left anterior descending (LAD). Then after an intravenous infusion of adenosine triphosphate, the velocity of blood flow was measured when the vessel was in maximal dilation. The ratio of flow velocity of those in maximal dilation to those at rest was CFVR. RESULTS: The subjects with a higher baPWV (> 1400 cm/s) were markedly elder and had higher risks of hypertension and diabetes. Thus age, hypertension and diabetes contributed to arteriosclerosis. More importantly, the subjects with a higher baPWV (> 1400 cm/s) had a much lower level of CFVR (2.66 ± 0.74 vs 2.95 ± 0.76; P < 0.01) than those with a lower baPWV (< 1400 cm/s). Furthermore correlation analysis showed that CFVR and baPWV levels were significantly negatively correlated (r = -0.35, P < 0.01). CONCLUSIONS: A negative correlation exists between artery stiffness and coronary flow velocity reserve. The increased vascular stiffness may impair coronary endothelial function, cause the dysfunction of coronary microcirculation and raise the risks of cardiovascular events.

Reduced local blood supply to the tibial metaphysis is associated with ovariectomy-induced osteoporosis in mice.

OBJECTIVE: To investigate angiogenesis of the tibial metaphysis in ovariectomized mice with microcomputed tomography, as well as to detect the expression of vascular endothelial growth factor (VEGF) in the metaphysis, and to explore the relationship between osteoporosis and local blood supply to bones. METHODS: Sixty mice were randomly divided into an ovariectomy group (n = 30) and a control group (n = 30). Four weeks after ovariectomy, the mice were killed and the distribution of vessels in the tibial metaphysis was determined after silicone rubber perfusion. In addition, the expression of VEGF of the tibial metaphysis was immunohistochemically determined and bone mineral density, microarchitecture, and biomechanics were tested. RESULTS: The bone mineral density, biomechanical parameters, number of microvessels, and expression of VEGF were significantly reduced in the tibial metaphysis of ovariectomized mice, whose bone microarchitecture was also disrupted. CONCLUSION: In this study, it was found that reduced local blood supply to the tibial metaphysis may be associated with ovariectomy-induced osteoporosis.

Methylprednisolone Induces Neuro-Protective Effects via the Inhibition of A1 Astrocyte Activation in Traumatic Spinal Cord Injury Mouse Models.

Traumatic spinal cord injury (TSCI) leads to pathological changes such as inflammation, edema, and neuronal apoptosis. Methylprednisolone (MP) is a glucocorticoid that has a variety of beneficial effects, including decreasing inflammation and ischemic reaction, as well as inhibiting lipid peroxidation. However, the efficacy and mechanism of MP in TSCI therapy is yet to be deciphered. In the present study, MP significantly attenuated the apoptotic effects of H2O2 in neuronal cells. Western blot analysis demonstrated that the levels of apoptotic related proteins, Bax and cleaved caspase-3, were reduced while levels of anti-apoptotic Bcl-2 were increased. In vivo TUNEL assays further demonstrated that MP effectively protected neuronal cells from apoptosis after TSCI, and was consistent with in vitro studies. Furthermore, we demonstrated that MP could decrease expression levels of IBA1, Il-1α, TNFα, and C3 and suppress A1 neurotoxic reactive astrocyte activation in TSCI mouse models. Neurological function was evaluated using the Basso Mouse Scale (BMS) and Footprint Test. Results demonstrated that the neurological function of MP-treated injured mice was significantly increased. In conclusion, our study demonstrated that MP could attenuate astrocyte cell death, decrease microglia activation, suppress A1 astrocytes activation, and promote functional recovery after acute TSCI in mouse models.

Percutaneous Endoscopic Transforaminal Lumbar Discectomy via Eccentric Trepan foraminoplasty Technology for Unilateral Stenosed Serve Root Canals.

OBJECTIVE: To evaluate the clinical outcomes of percutaneous lumbar foraminoplasty for unilateral stenosed nerve root canals. METHODS: The article is a retrospective analysis. From May 2016 to April 2017, 32 patients with lumbar spinal stenosis syndrome (unilateral stenosed nerve root canals) were treated with percutaneous endoscopic transforaminal lumbar discectomy (PETLD). The study included 15 men and 17 women, with an average age of 53.8 ± 15.4 years, ranging from 24 to 78 years. The indexes used for preoperative and postoperative 1 day, 3 months, and final follow up were the visual analogue scale (VAS) for lumbar and leg, the Oswestry disability index (ODI), and the modified Macnab criteria. All patients were followed up for an average 6 months after the operation. RESULTS: The average operative time was 75.82 ± 10.58 min, the average blood loss was 15.83 ± 3.75 mL, and the average hospital stay after surgery was 6.2 ± 4.6 days. The VAS score (leg) decreased from 6.94 ± 0.50 preoperatively to 1.16 ± 0.45 at the final follow up (P < 0.05) and ODI were obviously improved, from preoperative evaluation of 80.19 ± 5.55 to 9.44 ± 1.16 at the final follow up (P < 0.05). However, the postoperative VAS score (lumbar) did not show an improvement, reducing from 1.78 ± 0.49 preoperatively to 1.62 ± 0.55 at the final follow-up (P > 0.05). According to the modified Macnab criteria, the outcome showed that the excellent and good rate was 90.6%. There were three patients with hip soreness, and nerve root symptoms were relieved. CONCLUSION: Percutaneous endoscopic transforaminal lumbar discectomy has a satisfactory clinical effect in the treatment of lumbar spinal stenosis syndrome, especially for unilateral stenosed nerve root canals, and in decompressing the lateral recess and relieving the nerve root symptoms.

Circular RNA CirCHIPK3 promotes cell proliferation and invasion of breast cancer by sponging miR-193a/HMGB1/PI3K/AKT axis.

BACKGROUND: The aim of this study was to explore the potential mechanism of circular RNA (circRNA) CirCHIPK3 on the malignant proliferation and metastasis of breast cancer (BC). METHODS: Human BC samples and their matched normal adjacent tissues were obtained from 50 patients to assess the expression of CirCHIPK3 and its relationship with BC prognosis. A series of in vitro and in vivo functional experiments were carried out to elucidate the role of CirCHIPK3 in BC progression and its underlying molecular mechanisms. Moreover, the interaction of CirCHIPK3, miR-193a, and HMGB1 was examined using bioinformatics, FISH, RIP, RNA-pull down and luciferase reporter assays. Western blot analysis was performed to examine the expression of HMGB1, p-PI3K, total PI3K, p-AKT, and AKT after si-CirCHIPK3 transfection. RESULTS: Upregulation of CirCHIPK3 was identified in BC, which predicted a worse prognosis in BC patients. Furthermore, it was found that CirCHIPK3 facilitated cell proliferation, migration, and invasion in BC by regulating miR-193a/HMGB1/PI3K/AKT signaling. CirCHIPK3 acted as a sponge for miR-193a to facilitate HMGB1 expression. si-CirCHIPK3 also inhibited tumor growth of BC in nude mice. si-CircCHIPK3 decreased HMGB1/PI3K/AKT signal expression in MDA-MB-231 cells, whereas overexpression of CircCHIPK3 enhanced HMGB1/PI3K/AKT signal. CONCLUSIONS: CirCHIPK3 regulated miR-193a/HMGB1/PI3K/AKT signaling to facilitate BC development and progression, providing a novel therapeutic target for BC.

Gastrointestinal involvement of COVID-19 and potential faecal transmission of SARS-CoV-2.

Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was found initially in Wuhan, China in early December 2019. The pandemic has spread to 216 countries and regions, infecting more than 23310 000 people and causing over 800 000 deaths globally by Aug. 24, 2020, according to World Health Organization (https://www.who.int/emergencies/diseases/ novel-coronavirus-2019). Fever, cough, and dyspnea are the three common symptoms of the condition, whereas the conventional transmission route for SARS-CoV-2 is through droplets entering the respiratory tract. To date, infection control measures for COVID-19 have been focusing on the involvement of the respiratory system. However, ignoring potential faecal transmission and the gastrointestinal involvement of SARS-CoV-2 may result in mistakes in attempts to control the pandemic.

CXCL12/CXCR4 signaling contributes to neuropathic pain via central sensitization mechanisms in a rat spinal nerve ligation model.

BACKGROUND: Previous studies have demonstrated that the CXCL12/CXCR4 signaling axis is involved in the regulation of neuropathic pain (NP). Here, we performed experiments to test whether the CXCL12/CXCR4 signaling pathway contributes to the pathogenesis of neuropathic pain after spinal nerve ligation (SNL) via central sensitization mechanisms. METHODS: Neuropathic pain was induced and assessed in a SNL rat model. The expression and distribution of CXCL12 or CXCR4 were examined by immunofluorescence staining and western blot. The effects of CXCL12 rat peptide, CXCL12 neutralizing antibody, CXCR4 antagonist, and astrocyte metabolic inhibitor on pain hypersensitivity were explored by behavioral tests in naive or SNL rats. We measured the expression level of c-Fos and CGRP to evaluate the sensitization of neurons by RT-PCR. The activation of astrocyte and microglia was analyzed by measuring the level of GFAP and iba-1. The mRNA levels of the pro-inflammatory cytokines such as TNF-α, IL-1ß, and IL-6 and Connexin 30, Connexin 43, EAAT 1, EAAT 2 were also detected by RT-PCR. RESULTS: First, we found that the expression of CXCL12 and CXCR4 was upregulated after SNL. CXCL12 was mainly expressed in the neurons while CXCR4 was expressed both in astrocytes and neurons in the spinal dorsal horn after SNL. Moreover, intrathecal administration of rat peptide, CXCL12, induced hypersensitivity in naive rats, which was partly reversed by fluorocitrate. In addition, the CXCL12 rat peptide increased mRNA levels of c-Fos, GFAP, and iba-1. A single intrathecal injection of CXCL12 neutralizing antibody transiently reversed neuropathic pain in the SNL rat model. Consecutive use of CXCL12 neutralizing antibody led to significant delay in the induction of neuropathic pain, and reduced the expression of GFAP and iba-1 in the spinal dorsal horn. Finally, repeated intrathecal administration of the CXCR4 antagonist, AMD3100, significantly suppressed the initiation and duration of neuropathic pain. The mRNA levels of c-Fos, CGRP, GFAP, iba-1, and pro-inflammatory cytokines, also including Connexin 30 and Connexin 43 were decreased after injection of AMD3100, while EAAT 1 and EAAT 2 mRNAs were increased. CONCLUSION: We demonstrate that the CXCL12/CXCR4 signaling pathway contributes to the development and maintenance of neuropathic pain via central sensitization mechanisms. Importantly, intervening with CXCL12/CXCR4 presents an effective therapeutic approach to treat the neuropathic pain.

Preliminary results for the treatment of a pain-causing osteoporotic vertebral compression fracture with a Sky Bone Expander.

OBJECTIVE: Vertebral compression fractures (VCFs) are common complications of osteoporosis. The expansion of VCFs with a Sky Bone Expander is a new procedure which improves kyphotic deformities and decreases pain associated with VCFs. The purpose of this study was to investigate the preliminary results for the treatment of painful osteoporotic VCFs with a Sky Bone Expander. MATERIALS AND METHODS: Twenty-six patients with pain-causing VCFs were treated with a Sky Bone Expander. This operation involved the percutaneous insertion of the Sky Bone Expander into a fractured vertebral body transpedicularly. Following the expansion, the Sky Bone Expander was contracted and removed, resulting in a cavity to be filled with bone cement. All fractures were analyzed for improvement in sagittal alignment. Clinical complications, pain relief and ambulation status were evaluated 1 day, 1 week, 1 month, and 3 months after the operation. RESULTS: Twenty-four hours after the operation, all the patients treated experienced some degree of pain relief. In addition, no postoperative neurologic complications were noted. The average operative time was 42.4 +/- 15.5 min per vertebra. Moreover, an average cement volume of 3.5 mL (range, 2.5 +/- 5.0 mL) was injected per vertebra. The average anterior height was 18.4 +/- 5.1 mm preoperatively and 20.5 +/- 5.3 mm postoperatively (p < 0.01). Furthermore, the average midline height was 15.5 +/- 5.2 mm preoperatively and 18.9 +/- 4.0 mm postoperatively (p < 0.01). The Cobb angle improved from 18.5 +/- 8.2 degrees preoperatively to 9.2 +/- 4.0 degrees postoperatively (p < 0.01). The Visual Anabog Scale scores decreased from 7.7 +/- 1.8 points preoperatively to 3.1 +/- 2.0, 2.9 +/- 1.7, 2.6 +/- 1.5 and 2.9 +/- 11.3 after 1 day, 1 week, 1 month and 3 months after the operation, respectively. Cement extrusion was observed in four patients without any neurologic symptoms. CONCLUSION: As a result of this study, we can postulate that the expansion of compressed vetrebra with a Sky Bone Expander is a safe and minimally invasive procedure resulting in the restoration of vertebral body height and the relief of pain associated with VCFs.

Security and Radical Assessment in Open, Laparoscopic, Robotic Colorectal Cancer Surgery: A Comparative Study.

PURPOSE: This retrospective study was designed to assess the safety and effectiveness of open, laparoscopic, robotic colorectal cancer surgery. METHODS: Three hundred patients with colorectal cancer who underwent curative resection in the First Affiliated Hospital of Zhengzhou University between February 2014 and May 2016 were included. Patients were classified into open surgery group, laparoscopic surgery group, and robot-assisted group. RESULTS: The blood loss in laparoscopic surgery group was less than that in open surgery group, and the blood loss in robot-assisted group less was than the open surgery group. The number of lymph node dissection in robot-assisted group was significantly larger than that in the open group ( P < .05). The distance between the lower edge of the tumor group and the distal margin in robotic group was longer than that of the laparoscopic surgery group and the open group ( P < .05). Three (2.8%) cases of urinary retention occurred in the open surgery group, 4 (3.92%) cases in the laparoscopic surgery group, and 1 (1.1%) case in the robot-assisted group, while 2 (1.87%) cases of sexual dysfunction occurred in the open surgery group, 2 (1.96%) cases in the laparoscopic surgery group, and 1 (1.1%) case in the robot-assisted group. The urinary retention and sexual dysfunction rate did not differ between the 3 groups ( P > .05), but the minimally invasive group showed a certain advantage over the open group. CONCLUSION: Compared to the traditional open surgery, minimally invasive surgery (especially in robot-assisted group) has advantages such as less intraoperative bleeding, rapid postoperative recovery, and radical cure; open group, laparoscopic surgery group, and robot-assisted group have a similar incidence of postoperative complications, but reduction in the incidence of anastomotic leakage and intestinal obstruction. Robot-assisted group has the potential advantage for pelvic autonomic nerve protection.

Refractory hypotension induced by Sheehan syndrome with pituitary crisis: A case report.

The present study reported on an unusual case of refractory hypotension induced by Sheehan syndrome with pituitary crisis and explored the causes and treatment of hypotension in hypopiptuitarism. Refractory hypotension is a rare and severe complication of longstanding hypopituitarism induced by Sheehan syndrome with pituitary crisis. A 48-year-old Chinese woman with pituitary crisis due to Sheehan syndrome developed refractory hypotension and received longstanding vasopressor blood pressure support and hormone replacement therapy. Besides normalized blood pressure, echocardiography over 3 months revealed partial reversibility of her cardiac function with hormone replacement therapy. Consistent numerous studies reviewed, hormone replacement therapy may improve cardiac function in patients with cardiomyopathy linked to Sheehan syndrome. A retrospective study of 77 cases with hypopituitarism encountered at Qilu Hospital of Shandong University (Jinan, China) was also performed and the incidence rate of hypotension was analyzed, revealing that the present case was the first of refractory hypotension induced by Sheehan syndrome with pituitary crisis at this institution in 16 years.

miR-181d-5p promotes neurite outgrowth in PC12 Cells via PI3K/Akt pathway.

INTRODUCTION: miRNAs dysregulate in spinal cord injury (SCI) and have been demonstrated to play a crucial role in neurite outgrowth. However, the underlying mechanism remains elusive. In this study, we constructed a mouse model of SCI, extracted RNA from injured spinal cord tissue for the use of microarray assay. miR-181d-5p which is one of the most significantly expressed miRNAs in miRNA-mRNA network, abundantly expressed in center system and highly conserved across different spices, was chosen for our further study. AIMS: To demonstrate whether miR-181d-5p can promote neurite outgrowth in PC12 cells via PI3K/Akt signaling pathway, we performed function analysis of miR-181d-5p with LV-miR-181d-5p and LV-sh-GFP to infect PC12 cells. RESULTS: Through microarray assay analysis, we totally found 262 significantly expressed miRNAs and 2973 target genes in SCI and observed that their expression dynamically changed postinjury. Here, we provided enough evidences that the overexpression of miR181d-5p significantly decreased the expression of PTEN, upregulated p-Akt expression, increased neurite outgrowth-related proteins (GAP-43 and NF-200) and synaptic vesicle-related proteins (Synapsin and PSD95), and then promoted neurite outgrowth in PC12 cells. Furthermore, we confirmed that miR-181d-5p could directly target to the 3'-UTR of PTEN mRNA through dual-luciferase report assay. CONCLUSIONS: Our study supports that aberrant expression of miRNAs is involved in the pathogenesis of SCI, miR-181d-5p plays an important role in neurite growth in PC12 cells via PI3K/Akt signaling pathway and may be a candidate target for the treatment of SCI in the future.

POEMS syndrome presentation with progressive weakness in upper and lower limbs: A case report.

Polyneuropathy, organomegaly, endocrinopathy, M proteins, and skin changes (POEMS) syndrome is a rare variant of plasma cell disorders with multiple systemic manifestations. A 50-year-old female patient presented with progressive weakness in her upper and lower limbs; tingling, numbness and burning in her feet; polyneuropathy (demyelinating in the majority of cases of POEMS syndrome); monoclonal plasma cell disorder (typicallyλ-restricted in cases of POEMS syndrome); sclerotic lesions on the spine and pelvis; organomegaly, including hepatomegaly, splenomegaly and lymphadenopathy; edema; pleural effusion; adrenal, thyroidal, pituitary, gonadal and pancreatic endocrinopathy; skin changes, including hyperpigmentation, dry skin and hypertrichosis; thrombocytosis; pulmonary hypertension; low vitamin B12 and weight loss. Following the diagnosis of POEMS syndrome, the patient was treated only with pain-alleviating corticosteroids. Respiratory failure-induced mortality occurred 24 months after the patient first experienced difficulty walking and numbness in her lower extremities. The present study suggests that abnormal symptoms in cases of POEMS syndrome should be further evaluated during the diagnosis and treatment.

Long non-coding RNA LINC00959 predicts colorectal cancer patient prognosis and inhibits tumor progression.

Long non-coding RNAs (lncRNAs) are increasingly implicated in tumorigenesis and cancer progression. This study focused on the relationship between the lncRNA LINC00959 and colorectal cancer (CRC). We found that LINC00959 expression was lower in CRC tissues than normal colorectal mucosae. High LINC00959 expression was negatively associated with TNM stage, distant metastasis, and lymphatic metastasis, and correlated with a better prognosis in 87 CRC cases. In vitro, LINC00959 knockdown enhanced colon cancer cell proliferation, invasion, and migration; upregulated N-cadherin and vimentin; and downregulated E-cadherin and Caspase-3. LINC00959 overexpression produced the opposite effects. These data suggest that LINC00959 inhibits tumor cell invasion and migration by suppressing epithelial-mesenchymal transition and promotes apoptosis through Caspase-3. LINC00959 may be a tumor suppressor and useful prognostic biomarker in CRC.