Associations of four surrogate insulin resistance indexes with non-alcoholic steatohepatitis in Chinese patients with obesity: a cross-sectional study.

OBJECTIVES: This study was designed to evaluate the association of four surrogate indexes of IR with NASH in patients with obesity. METHODS: A total of 270 patients who underwent bariatric surgery, were included in this cross-sectional study. NASH was diagnosed based on liver biopsies. Binary logistics regression analyses were performed to assess the associations of four surrogate indexes of IR (HOMA-IR, Matsuda index, TyG, and TG/HDL-C) with NASH in patients with obesity. The restricted cubic spline was used to assess the dose-response associations of surrogate indexes of IR with NASH after adjusting for confounding factors. RESULTS: NASH was diagnosed in 136 patients, with a prevalence of 50.37%. Compared with tertile 1, the fully adjusted ORs (95% CIs) of NASH for tertile 3 were 2.711(1.113-6.608) and 0.297 (0.152-0.579) for TyG and Matsuda index. Consistently, per SD increment of TyG were still significantly associated with 64% increased risks of NASH, and per SD increment of Matsuda index were still significantly associated with 38% decreased risks of NASH. In contrast, no significant associations were found between HOMA-IR and TG/HDL-C and the risk of NASH in patients with obesity (all P > 0.05). After adjusting covariates in restricted cubic splines, the risk of NASH decreased with the increment of Matsuda Index levels (P-nonlinear = 0.442, P-overall = 0.007) and with the decrement of TyG levels (P-nonlinear = 0.004, P-overall = 0.001). CONCLUSIONS: In patients with obesity, TyG and Matsuda index were independently related to the risk of NASH after adjustment for traditional risk factors. In addition, compared with HOMA-IR and TG/HDL-C, the Matsuda index and TyG may be more suitable for NASH prediction in patients with obesity.

MiR-506 Promotes Antitumor Immune Response in Pancreatic Cancer by Reprogramming Tumor-Associated Macrophages toward an M1 Phenotype.

Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant cancer with a poor prognosis, and effective treatments for PDAC are lacking. In this study, we hypothesized that miR-506 promotes antitumor immune response in PDAC by reprogramming tumor-associated macrophages toward an M1 phenotype to reverse its immunosuppressive tumor microenvironment (TME). First, the relationship between TME and the expression of miR-506 was assessed using clinical samples. Our results provided evidence that lower expression of miR-506 was associated with poor prognosis and immunosuppressive TME in PDAC patients. In addition, miR-506 inhibit the PDAC progression and reversed its immunosuppressive microenvironment in a macrophage-dependent manner. Next, we established a PDAC mouse model by orthotopic injection to further explore the role of miR-506 in vivo. Mechanistic investigations demonstrated that miR-506 could reprogram the polarization of M2-like macrophages toward an M1-like phenotype through targeting STAT3. Meanwhile, miR-506 could also sensitize PDAC to anti-PD-1 immunotherapy, because the tumor microenvironment remodeling effects of miR-506 could reprogram macrophage polarization and subsequently promote cytotoxic T lymphocyte (CTL) infiltration. These findings suggest a relationship between miR-506 and TME, especially M2-like macrophages, thus providing novel insights into mechanisms of tumor progression and potential immunotherapeutic targets for further clinical treatment.

Development, Validation, and Application of a Scoring Model for Non-alcoholic Steatohepatitis.

PURPOSE: The aim of this study was to explore risk factors of NASH and then develop a non-invasive scoring model in Chinese patients with obesity. A scoring system was then applied to assess the effect of sleeve gastrectomy on NASH. METHODS: A total of 243 patients with obesity were included and divided into NASH group and non-NASH group according to the pathological results of liver biopsy. Logistic regression was used to determine risk factors of NASH. A scoring model was derived by risk factors of NASH. Then, postoperative follow-up was performed in 70 patients. RESULTS: Among the 243 patients, 118 (48.56%) patients showed NASH. Multivariate logistic regression identified aspartate aminotransferase (AST) (>21.50 IU/L), high-density lipoprotein cholesterol (HDL-C) (<1.155mmol/L), and homeostasis model assessment (HOMA-IR) (>9.368) as independent risk factors of NASH. The model included above risk factors showed a negative predictive value (NPV) of 70.38% in the low-risk category and a positive predictive value (PPV) of 85.71% in the high-risk category, with the area under the receiver operator curve (AUROC) of 0.737. Bariatric surgery resulted in a sharp decline in AST and HOMA-IR and a significant increase of HDL-C. The points of scoring model were improved at 6 months after surgery. CONCLUSION: A non-invasive scoring model was derived by the risk factors of NASH included AST, HDL-C, and HOMA-IR and applied to the postoperative follow-up. After sleeve gastrectomy, the above risk factors and points of scoring model were significantly improved.

Insulin Resistance, but Not Obstructive Sleep Apnea Is Associated with Hepatic Steatosis in Chinese Patients with Severe Obesity.

INTRODUCTION: Severe obesity is often present with non-alcoholic fatty liver disease (NAFLD) and obstructive sleep apnea (OSA). Emerging researches suggest OSA plays an important role in NAFLD development and progression while the relationship between OSA and NAFLD is still conflicting. The interaction of OSA and NAFLD should be further evaluated as obesity surges. The purpose of this study was to assess the prevalence of OSA and NAFLD in patients with obesity undergoing bariatric surgery and evaluate the association between OSA and severity of NAFLD. METHODS: 141 patients with severe obesity undergoing preoperative polysomnography and intraoperative liver biopsy during bariatric surgery were investigated. Clinical, anthropometric variables, liver enzymes, fasting blood glucose, fasting serum insulin, and homeostasis model assessment of insulin resistance (HOMA-IR) were measured. The severity of NAFLD was assessed by degree of steatosis, ballooning, intralobular inflammation, and NAFLD activity score. The diagnosis and severity assessment of OSA was based on an apnea/hypopnea index (AHI). RESULTS: OSA was diagnosed in 127 (90.07%), NAFLD in 124 (87.94%), and non-alcoholic steatohepatitis in 72 (51.06%) patients. There was a statistical difference in BMI, waist circumstance, neck circumstance, high-density lipoprotein cholesterol, fasting insulin, and HOMA-IR among the three groups divided by the severity of AHI. In addition, the distribution of hepatic steatosis grades among the three groups was statistically different (p = 0.025). AHI was significantly associated with HOMA-IR and hepatic steatosis when assessing the association between OSA parameters and liver histology in NAFLD (p < 0.05). Patients with steatosis of grades 1-3 had significantly elevated aspartate aminotransferase, alanine aminotransferase, gamma glutamyl transferase, triglycerides, fasting insulin, fasting glucose, HOMA-IR, and AHI compared with the patients with steatosis of grade 0. In a multivariable logistic analysis, the positive association between AHI and hepatic steatosis attenuated after adjusting for HOMA-IR. CONCLUSION: Prevalence of OSA and NAFLD was high in patients with obesity eligible for bariatric procedures. HOMA-IR, but not AHI, was an independent risk factor for hepatic steatosis in this population.

Crosstalk between autophagy and immune cell infiltration in the tumor microenvironment.

Autophagy is a conserved process for self-degradation and provides cells with a rescue mechanism to respond to circumstances such as stress and starvation. The role of autophagy in cancer is extremely complex and often paradoxical. Most of the related published studies on tumors are always focused on cancer cells. However, present studies gradually noticed the significance of autophagy in the tumor microenvironment. These studies demonstrate that autophagy and immunity work synergistically to affect tumor progression, indicating that autophagy could become a potential target for cancer immunotherapy. Therefore, it is crucial to clarify the correlation between autophagy and various tumor-infiltrating immune cells in the tumor microenvironment. The context-dependent role of autophagy is critical in the design of therapeutic strategies for cancer.

IGFBP2 Drives Regulatory T Cell Differentiation through STAT3/IDO Signaling Pathway in Pancreatic Cancer.

Pancreatic ductal adenocarcinoma (PDAC) represents one of the deadliest malignancies. Elevated regulatory T cell (Treg) infiltration has a potent immunosuppressive function in tumor biology, which contributes to low survival in PDAC. Nonetheless, the crosstalk between malignant cells and tumor-infiltrating Tregs in PDAC is not well understood. Here, clinical data demonstrates that the insulin-like growth factor binding protein 2 (IGFBP2) is associated with Treg accumulation in the microenvironment of PDAC in humans. Additionally, IGFBP2 increases Treg infiltration in the tumor microenvironment and promotes disease progression in mouse PDAC. Bioinformatic analysis and mechanistic assessment reveals IGFBP2 upregulated indoleamine 2, 3-dioxygenase (IDO) by activating signal transducer and activator of transcription 3 (STAT3) signaling in PDAC cells, thus inducing Treg differentiation and an immunosuppressive tumor microenvironment. These findings provide mechanistic insights into an important molecular pathway that promotes an immunosuppressive microenvironment, which suggests the IGFBP2 axis as a potential target for improved immune response in PDAC.

Associations among FT4 level, FT3/FT4 ratio, and non-alcoholic fatty liver disease in Chinese patients with hypopituitarism.

Non-alcoholic fatty liver disease (NAFLD) is the most common hepatic metabolic disorder. Thyroid function is associated with NAFLD in different populations; however, little attention has been paid in patients with hypopituitarism. To analyze the association between thyroid function and NAFLD, we included 134 patients with hypopituitarism admitted to the Tianjin Medical University General Hospital between June 2013 and May 2019. Participants were divided into the NAFLD(-) and NAFLD(+) groups based on abdominal ultrasonography findings. We evaluated 68 male and 66 female patients with hypopituitarism. The prevalence of NAFLD was 52.24%. The NAFLD(+) group had a significantly higher free triiodothyronine/free thyroxine (FT3/FT4) ratio than the NAFLD(-) group (p = 0.003). The NAFLD(+) group showed significantly lower levels of FT4 and the growth hormone (GH) than the NAFLD(-) group (p = 0.003 and 0.016, respectively). We observed an association of the FT4 level and FT3/FT4 ratio with NAFLD in the univariate model, which was non-significant after adjustment for metabolic parameters (BMI, HDL-C, triglycerides, serum uric acid, blood pressure, fasting glucose). To better understand the role of each metabolic parameters, we performed additional models for each of those predictors individually after adjustment for age and gender, the association between FT4 level and FT3/FT4 ratio lost significance after adjustment for HDL-C and TG, but not for other predictors. Our findings suggest that thyroid dysfunction may be crucially involved in NAFLD by regulating whole-body metabolism, especially lipid utilization. Therefore, sufficient thyroid hormone replacement therapy for patients with hypopituitarism is recommended from the early stage.

Relationship Between Sleep-Wake Disturbance and Risk of Malnutrition in Hospitalized Patients With Cirrhosis.

Both sleep-wake disturbance and malnutrition are common in cirrhosis and might be associated with similar adverse outcomes, such as impaired health-related quality of life, hepatic encephalopathy, and sarcopenia, but there is no study investigating the relationship between these two. We aimed to explore the relationship between sleep-wake disturbance [estimated by the Pittsburgh Sleep Quality Index (PSQI)] and malnutrition risk [estimated by the Royal Free Hospital-Nutritional Prioritizing Tool (RFH-NPT)]. About 150 patients with cirrhosis were prospectively recruited. The nutritional risk is classified as low (0 points), moderate (1 point), and high (2-7 points) according to the RFH-NPT score. A global PSQI >5 indicated poor sleepers. Furthermore, multivariate linear regression analyses were performed to determine the relationship between sleep-wake disturbance and malnutrition. The median PSQI was seven, and RFH-NPT was two in the entire cohort, with 60.67 and 56.67% rated as poor sleep quality and high malnutrition risk, respectively. Patients with cirrhosis with poor sleep quality had significantly higher RFH-NPT score (3 vs. 1, P = 0.007). Our multivariate analyses indicated that male patients (ß = 0.279, P < 0.001), ascites (ß = 0.210, P = 0.016), and PSQI (ß = 0.262, P = 0.001) were independent predictors of malnutrition. In addition, the differences regarding PSQI score were more significant in male patients, as well as those >65 years or with Child-Turcotte-Pugh class A/B (CTP-A/B) or the median model for end-stage liver disease (MELD) <15. Taken together, the sleep-wake disturbance is strongly correlated with high malnutrition risk in patients with cirrhosis. Given sleep-wake disturbance is remediable, it is tempting to incorporate therapies to reverse poor sleep quality for improving nutritional status in patients with cirrhosis.

IGFBP2 promotes tumor progression by inducing alternative polarization of macrophages in pancreatic ductal adenocarcinoma through the STAT3 pathway.

Tumor-associated macrophages (TAMs) represent the M2-like phenotype with potent immunosuppressive activity, and play a pro-tumor role in pancreatic ductal adenocarcinoma (PDAC) biology. In this study, we investigated the role of the insulin-like growth factor binding protein 2 (IGFBP2) as a determinant of TAM polarity. Clinical data revealed that the levels of IGFBP2 correlated with M2 TAMs accumulation and disease progression in human PDAC. In vivo mouse model experiments showed that IGFBP2 promoted an immunosuppressive microenvironment and tumor growth in a macrophage dependent manner. Bioinformatics analysis of PDAC transcriptomes revealed a significant association between IGFBP2 expression and M2 macrophage polarization and signal transducer and activator of transcription 3 (STAT3) activation. Mechanistic investigations demonstrated that IGFBP2 augmented the expression and secretion of IL-10 through STAT3 activation in PDAC cells, which induced TAM polarization toward an M2 phenotype. IGFBP2-polarized M2 macrophages significantly increased Tregs infiltration and impaired antitumor T-cell immunity in a mouse model. Thus, our investigations have illuminated the IGFBP2 signaling pathway that contributes to the macrophage-based immunosuppressive microenvironment in PDAC, suggesting that blocking the IGFBP2 axis constitutes a potential treatment strategy to reset TAM polarization toward an antitumor state in PDAC.

Exon 3 mutations of CTNNB1 drive tumorigenesis: a review.

The canonical Wnt/ß-catenin signaling pathway, an important modulator of progenitor cell proliferation and differentiation, is highly regulated for the maintenance of critical biological homeostasis. Decades of studies in cancer genetics and genomics have demonstrated that multiple genes encoding key proteins in this signaling pathway serve as targets for recurrent mutational alterations. Among these proteins, ß-catenin and adenomatosis polyposis coli (APC) are two key nodes. ß-catenin contributes in transporting extracellular signals for nuclear programming. Mutations of the CTNNB1 gene that encodes ß-catenin occur in a wide spectrum of cancers. These mutations alter the spatial characteristics of the ß-catenin protein, leading to drastic reprogramming of the nuclear transcriptional network. Among the outcomes of this reprogramming are increased cell proliferation, enhanced immunosuppression, and disruption of metabolic regulation. Herein we review the current understanding of CTNNB1 mutations, their roles in tumorigenesis and discuss their possible therapeutic implications for cancer.

MIR506 induces autophagy-related cell death in pancreatic cancer cells by targeting the STAT3 pathway.

Pancreatic ductal adenocarcinoma (PDAC) is the most aggressive and lethal cancer. The role of autophagy in the pathobiology of PDAC is intricate, with opposing functions manifested in different cellular contexts. MIR506 functions as a tumor suppressor in many cancer types through the regulation of multiple pathways. In this study, we hypothesized that MIR506 exerted a tumor suppression function in PDAC by inducing autophagy-related cell death. Our results provided evidence that downregulation of MIR506 expression was associated with disease progression in human PDAC. MIR506 triggered autophagic flux in PDAC cells, which led to autophagy-related cell death through direct targeting of the STAT3 (signal transducer and activator of transcription 3)-BCL2-BECN1 axis. Silencing and inhibiting STAT3 recapitulated the effects of MIR506, whereas forced expression of STAT3 abrogated the effects of MIR506. We propose that the apoptosis-inhibitory protein BCL2, which also inhibits induction of autophagy by blocking BECN1, was inhibited by MIR506 through targeting STAT3, thus augmenting BECN1 and promoting autophagy-related cell death. Silencing BECN1 and overexpression of BCL2 abrogated the effects of MIR506. These findings expand the known mechanisms of MIR506-mediated tumor suppression to activation of autophagy-related cell death and suggest a strategy for using MIR506 as an anti-STAT3 approach to PDAC treatment.

Clinicopathological and prognostic significance of cancer stem cell markers CD44 and CD133 in patients with gastric cancer: A comprehensive meta-analysis with 4729 patients involved.

BACKGROUND: In recent years, CD44 and CD133 have been identified as 2 common used cancer stem cell (CSC) markers in gastric cancer. However, the clinicopathological and prognostic value of these markers in gastric cancer remains controversial; moreover, there is lack of comparison of these 2 markers' roles in clinical applications. A systematic review and meta-analysis was conducted to elucidate these markers' clinicopathological features and association with prognosis in patients with gastric cancer. METHODS: Eligible studies were identified and odds ratios (ORs), hazard ratios (HRs) with 95% confidence intervals (CIs) were estimated. Heterogeneity and sensitivity were analyzed as well. Publication bias was assessed using funnel plots and Egger tests. RESULTS: The meta-analysis included 26 studies involving 4729 patients. High expression of CD44 was associated with Lauren type (intestinal type) (OR, 1.53 [95% CI, 1.02-2.30]; P = 0.038) and lymphatic vessel invasion (OR, 1.36 [95% CI, 1.06-1.76]; P = 0.021). CD133 overexpression was related to high TNM stage (III/IV) (OR, 3.18 [95% CI, 2.48-4.07]; P = 0.000), high depth of invasion (T3/T4) (OR, 2.97 [95% CI, 2.20-4.03]; P = 0.000), lymph node metastasis (OR, 2.82 [95% CI, 2.16-3.69]; P = 0.000), vascular invasion (OR, 6.71 [95% CI, 1.63-27.63]; P = 0.008), and distant metastasis (OR, 2.32 [95% CI, 1.64-3.29]; P = 0.000). In addition, survival analysis demonstrated a significant association between CD44, as well as CD133 and poor 5-year overall survival (HR, 1.87 [95% CI, 1.55-2.26]; P = 0.000; HR, 2.07 [95% CI, 1.76-2.44]; P = 0.000, respectively). CONCLUSION: These data suggest that upregulated expression of CD44 and CD133 correlates with several clinicopathological features and poor prognosis. Since the related features do not overlap, combined detection of CD44 and CD133 expression can be an especially effective tool for pathological diagnosis and prognostic prediction of gastric cancer patients in clinical applications.

Microwave ablation-assisted liver gene transfection in rats.

PURPOSE: Thermal ablation has been used to manage liver malignancy. This study aimed to assess histological changes in rat liver after microwave ablation (MWA) and to investigate whether thermal damage caused by MWA on surrounding liver tissue enhances the efficiency of liver gene transfer. METHODS: MWA was applied to rat liver, and the pathological tissue and ultrastructural changes were evaluated. Green fluorescent protein (GFP) and Renilla luciferase-expressing plasmids were administered to liver tissues by direct injection. GFP expression in liver tissue was analysed in frozen sections using an inverted fluorescence microscope, and Renilla luciferase expression in target tissue was determined using a luminometer. RESULTS: Tissue demarcations were observed in liver tissue after ablation, and a transition zone with morphological changes was present between necrotic and normal tissue. Hepatocytes in the transition zone showed decreased numbers of microvilli on cell surfaces and increased extracellular space. GFP expression was observed in the transition zone after MWA and plasmid injection and lasted up to 7 days post-ablation. Both the fluorescence and luminescence levels in the transition zone of the liver tissue were significantly higher than those in the untreated tissue (P < 0.001). CONCLUSIONS: Direct plasmid injection to the liver tissue of the transition zone after MWA can achieve effective gene transfection. These findings provide an experimental basis for exploring MWA-assisted target gene transfer for cancer gene therapy.

Artificial antigen-presenting cells expressing AFP(158-166) peptide and interleukin-15 activate AFP-specific cytotoxic T lymphocytes.

Professional antigen-presenting cells (APCs) are potent generators of tumor antigen-specific cytotoxic T lymphocytes (CTLs) for adoptive immunotherapy; however, generation of APCs is cumbersome, expensive, and subject to the tumor microenvironment. Artificial APCs (aAPCs) have been developed as a cost-effective alternative to APCs. We developed a cellular aAPC that efficiently generated alpha-fetoprotein (AFP)-specific CTLs. We genetically modified the human B cell lymphoma cell line BJAB with a lentiviral vector to establish an aAPC called BA15. The expression of AFP(158-166)-HLA-A*02:01 complex, CD80, CD86, and interleukin (IL)-15 in BA15 cells was assessed. The efficiency of BA15 at generating AFP-specific CTLs and the specific cytotoxicity of CTLs against AFP+ cells were also determined. BA15 cells expressed high levels of AFP(158-166) peptide, HLA-A2, CD80, CD86, and IL-15. BA15 cells also exhibited higher efficiency in generating AFP-specific CTLs than did dendritic cells. These CTLs had greater cytotoxicity against AFP+ hepatocellular carcinoma cells than did CTLs obtained from dendritic cells in vitro and in vivo. Our novel aAPC system could provide a robust platform for the generation of functional AFP-specific CTLs for adoptive immunotherapy of hepatocellular carcinoma.

Engineered cytotoxic T lymphocytes with AFP-specific TCR gene for adoptive immunotherapy in hepatocellular carcinoma.

Alpha-fetoprotein (AFP) is overexpressed in hepatocellular carcinoma (HCC) and could serve as a tumor-associated antigen (TAA) and potential target for adoptive immunotherapy. However, low frequency and severe functional impairment of AFP-specific T cells in vivo hamper adoptive infusion. TAA-specific T cell receptor (TCR) gene transfer could be an efficient and reliable alternation to generate AFP-specific cytotoxic T lymphocytes (CTLs). Autologous dendritic cells (DC) pulsed with AFP158-166 peptides were used to stimulate AFP-specific CTLs. TCR α/ß chain genes of AFP-specific CTLs were cloned and linked by 2A peptide to form full-length TCR coding sequence synthesized into a lentiviral vector. Nonspecific activated T cells were engineered by lentivirus infection. Transgenetic CTLs were evaluated for transfection efficiency, expression of AFP158-166-specific TCR, interferon (IFN)-γ secretion, and specific cytotoxicity toward AFP+ HCC cells in vitro and in vivo. Flow cytometry revealed the AFP158-166-MHC-Pentamer positive transgenetic CTLs was 9.86 %. The number of IFN-γ secretion T cells and the specific cytotoxicity toward HpeG2 in vitro and in tumor-bearing NOD/SCID mice were significantly raised in transgenetic CTLs than that of AFP158-166-specific CTLs obtained by peptide-pulsed DCs or control group. TCR gene transfer is a promising strategy to generate AFP158-166-specific CTLs for the treatment of HCC.

MicroRNA Signaling Pathway Network in Pancreatic Ductal Adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is considered to be the most lethal and aggressive malignancy with high mortality and poor prognosis. Their responses to current multimodal therapeutic regimens are limited. It is urgently needed to identify the molecular mechanism underlying pancreatic oncogenesis. Twelve core signaling cascades have been established critical in PDAC tumorigenesis by governing a wide variety of cellular processes. MicroRNAs (miRNAs) are aberrantly expressed in different types of tumors and play pivotal roles as post-transcriptional regulators of gene expression. Here, we will describe how miRNAs regulate different signaling pathways that contribute to pancreatic oncogenesis and progression.

Gastric bronchogenic cyst presenting as a gastrointestinal stromal tumor.

Bronchogenic cyst (BC) is congenital abnormality of the tracheobronchial bud derived from the primitive foregut which is predominantly found in the mediastinum. Surgery remains the most common treatment when malignancy is suspected, or when there are presenting. Only infrequently, is BC located at an extrathoracic site. Although rarely located in the stomach, BC should be considered as a differential diagnosis of gastric neoplasm. For these cases, surgery remains a common choice. Minimally invasive procedures such as endoscopic ultrasonography-guided fine needle biopsy aspiration (EUS-FNA) and endoscopic submucosal dissection (ESD) should also be considered when the diagnosis of BC is suspected. They are valuable diagnostic methods that can assess and identify the location of the lesion, and facilitate histological examination of the cyst. In some cases of more superficial lesions ESD can take the place of surgery as it avoids unnecessary complications of a more invasive procedure. Here we present a case of gastric BC located in the fundus of the stomach that resembled a gastrointestinal stromal tumor (GIST). We discuss its embryology, pathogenesis, radiological, clinical and treatment modalities. We also provide a thorough review of 14 cases (including our own case), which completely meet pathological criteria has been undertaken focusing on symptom, location, treatment, and histological features.

Preoperative serum alkaline phosphatase: a predictive factor for early hypocalcaemia following parathyroidectomy of primary hyperparathyroidism.

BACKGROUND: Postoperative hypocalcemia is one of the most common complications following parathyroidectomy for primary hyperparathyroidism (PHPT). The aim of this study was to analyze the predictive value of biochemical parameters as indicators for episodes of hypocalcemia in patients undergoing parathyroidectomy for PHPT. METHODS: The patients with PHPT who underwent parathyroidectomy between February 2004 and February 2014 were studied retrospectively at a single medical center. The patients were divided into biochemical, clinical, and no postoperative hypocalcemia groups, based on different clinical manifestations. Potential risk factors for postoperative hypocalcemia were identified and investigated by univariate and multivariate Logistic regression analysis. RESULTS: Of the 139 cases, 25 patients (18.0%) were diagnosed with postoperative hypocalcemia according to the traditional criterion. Univariate analysis revealed only alkaline phosphatase (ALP) and the small area under the curve (AUC) of receiver operating characteristics (ROC) curve for ALP demonstrates low accuracy in predicting the occurrence of postoperative hypocalcemia. Based on new criteria, 22 patients were added to the postoperative hypocalcemia group and similar biochemical parameters were compared. The serum ALP was a significant independent risk factor for postoperative hypocalcemia (P = 0.000) and its AUC of ROC curve was 0.783. The optimal cutoff point was 269 U/L and the sensitivity and specificity for prediction were 89.2% and 64.3%, respectively. CONCLUSIONS: The risk of postoperative hypocalcemia after parathyroidectomy should be emphasized for patients with typical symptoms of hypocalcemia despite their serum calcium level is in normal or a little higher range. Serum ALP is a predictive factor for the occurrence of postoperative hypocalcemia.

Emergency caudate lobectomy for ruptured hepatocellular carcinoma with multiple primary cancers.

We report a case of metachronous multiple primary malignancies involving both rectum and liver with colonic metastasis from hepatocellular carcinoma (HCC) through hematogenous pathway. A 72-year-old woman was admitted to the emergency department with right upper abdominal pain for 4 h. Considering her surgical history of Mile's procedure plus liver resection for rectal cancer with liver metastasis three years ago and the finding of urgent computed tomography scan on admission, the preoperative diagnosis was spontaneous rupture of rectal liver metastasis located in caudate lobe and colonic metastasis from rectal cancer. The patient underwent an emergency isolated caudate lobectomy at a hemorrhagic shock status. Pathology reported a primary HCC in the caudate lobe and colonic metastasis of HCC with tumor embolus in the surrounding vessels of the intestine. No regional lymph node involvement was found. It is hypothesized that HCC may disseminate hematogenously to the ascending colon, thus making it a rare case.

[Interventional effect of behaviour psychotherapy on patients with premature ejaculation].

OBJECTIVE: To investigate the interventional effect of comprehensive behaviour psychotherapy on the ejaculatory latency of premature ejaculation (PE) patients, sexual satisfaction of sexual partners, as well as its influence on the results of clinical treatment. METHODS: Ninety PE patients were randomly divided into a psychological intervention group (n = 45) and a control group (n = 45). Both groups were given medicine therapy, and the former also received comprehensive behaviour psychotherapy for 6 weeks. All the patients were assessed with the Chinese index of sexual function for PE and ejaculatory latency in the vagina, and the clinical efficacy was compared between the two groups. RESULTS: Before treatment, the ejaculatory latency in the vagina was (0.69 +/- 0.25) min and (0.71 +/- 0.19) min respectively in the intervention and the control groups, as compared with (5.87 +/- 0.59) min and (4.76 +/- 0.54) min before treatment, with significant difference (P < 0.01). In the intervention group, the scores in the control of ejaculatory reflex, the sexual satisfaction of the patients and their sexual partners and anxiety or depress in sexual activity in CIPE were higher than in the control group, with significant difference between the two groups (t = 2.12, 2.31, 2.01, 2.24, P < 0.05). The difference in the SAS score after therapy was of significance (P < 0.01). A month after treatment, the effectivity rates of the two groups were 82.9% and 30% respectively, and the difference was significant (P < .01). CONCLUSION: Comprehensive behaviour psychotherapy obviously adds to the clinical efficacy of drugs in the treatment of PE.