Climate Variability and Avian Cholera Transmission in Guangxi, China

In recent years, Guangxi has become one of the most severely affected provinces by epidemics of avian cholera in China. To date, the major determinant climatic factors of the disease in the region have remained largely unknown, making it difficult to effectively target countermeasures for avian cholera surveillance and control. This study aimed to quantify the relationship between climatic variables and cases of avian cholera in subtropical areas of China. Data relating to local meteorological variables and notified cases of avian cholera were supplied by the relevant authorities between January 2006 and December 2015. Spearman correlation, co-linearity statistics and cross-correlation analysis were applied to the data, controlling for co-linearity and lag effects. A time-series Poisson regression analysis was conducted to examine the degree of correlation between the climate variables and avian cholera transmission. The results indicated that monthly mean temperature, relative humidity, rainfall and the multivariate El Niño Southern Oscillation Index, with 2-3 months lag, were correlated with avian cholera incidence. The final model had good predictive ability for the occurrence of avian cholera. Overall, the findings indicate that climate variability plays an important role in avian cholera transmission in Guangxi province. Adoption of the model presented in this study could usefully inform avian cholera surveillance strategies, making them significantly simpler and more effective. The model could also serve as a decision support tool for veterinary professionals and health authorities.(AU)

Climate Variability and Avian Cholera Transmission in Guangxi, China

In recent years, Guangxi has become one of the most severely affected provinces by epidemics of avian cholera in China. To date, the major determinant climatic factors of the disease in the region have remained largely unknown, making it difficult to effectively target countermeasures for avian cholera surveillance and control. This study aimed to quantify the relationship between climatic variables and cases of avian cholera in subtropical areas of China. Data relating to local meteorological variables and notified cases of avian cholera were supplied by the relevant authorities between January 2006 and December 2015. Spearman correlation, co-linearity statistics and cross-correlation analysis were applied to the data, controlling for co-linearity and lag effects. A time-series Poisson regression analysis was conducted to examine the degree of correlation between the climate variables and avian cholera transmission. The results indicated that monthly mean temperature, relative humidity, rainfall and the multivariate El Niño Southern Oscillation Index, with 2-3 months lag, were correlated with avian cholera incidence. The final model had good predictive ability for the occurrence of avian cholera. Overall, the findings indicate that climate variability plays an important role in avian cholera transmission in Guangxi province. Adoption of the model presented in this study could usefully inform avian cholera surveillance strategies, making them significantly simpler and more effective. The model could also serve as a decision support tool for veterinary professionals and health authorities.

Computed Tomography Identifies Hepatic Portal Venous Gas Caused by Severe Diarrhoea.

AIM: To use computed tomography (CT) to diagnose the reasons for hepatic portal venous gas (HPVG) in the case of an elderly male patient. METHODS: This is a case study of an elderly male patient who suffered acute, obvious abdominal pain accompanied with stop of exhaust defecation following three days of diarrhoea, abdominal distention and emesis. The patient also developed asthma, which gradually became severe. The patient was admitted to the hospital where he underwent a physical examination and a CT scan. RESULTS: The CT results confirmed that the patient was suffering from HPVG caused by severe diarrhoea. The CT scan showed obvious expansion and pneumatosis in the enteric cavity and subcutaneous emphysema in the intestinal wall. Also, the intrahepatic portal branches and small branches of veins in the mesentery were filled with a high density of gas. The combination of many factors led to HPVG. Gastrointestinal mucosa and pressure accompanied with intestinal septic infection were the main factors. The case report revealed that gas in the enteric cavity went into the submucosa, then into the small branches of veins in the mesentery and finally into the intrahepatic portal vein system. CONCLUSIONS: Computed examination revealed the imaging features of HPVG. Hepatic portal venous gas suggested the growth of enteric cavity pressure, the damage of intestinal mucosa and intestinal infection, providing references for clinical diagnosis.

Variations in WNT3 gene are associated with incidence of non-syndromic cleft lip with or without cleft palate in a northeast Chinese population.

Non-syndromic cleft lip with or without cleft palate (NSCL/P) is a common birth defect. Several WNT genes are involved in craniofacial embryogenesis, and therefore may play an important role in the etiology of NSCL/P. Two SNPs (rs3809857 and rs9890413) in the WNT3 gene were subjected to case-control and case-parent analysis by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 236 unrelated patients with NSCL/P, including 128 elementary families (185 mothers and 154 fathers), and 400 control individuals from northeast China. The rs3809857 SNP, under the assumption of a dominant model, was found to induce a 2-fold lower risk of NSCL/P ORGG vs GT + TT = 0.605, 95%CI = 0.436-0.839, P = 0.003). Moreover, the family-based association test revealed an under-transmission for the minor allele T. On the other hand, we observed a significant association in the case-control and case-parent analysis of the SNP rs9890413. In addition, the P values for the haplotype of rs3809857-rs9890413 were observed to be statistically significant (P = 0.004). In conclusion, our study confirmed the association between the WNT3 variant and NSCL/P in the population tested.

Effect of low temperatures on BAX and BCL2 proteins in rats with spinal cord ischemia reperfusion injury.

We evaluated changes in BAX and BCL2 expression levels after spinal cord ischemia/reperfusion injury (SCII) and hypothermia during operations in rats. Eighty rats were divided into four groups: Group A (N = 20, 18°C); Group B (N = 20, 28°C); Group C (N = 20, room temperature); and Group D (N = 20, sham operation control). Spinal cord ischemia was induced for 90 min. Hypothermia was induced 15 min before, and maintained during ischemia, followed by heating to normothermia for 30 min after reperfusion. Motor function of the lower limbs was evaluated according to the Tarlov score at 72 and 168 h. For each rat, spinal cord samples were taken at 6, 24, 72 h, and 1 week to evaluate the histopathological changes, neuronal apoptosis, and BAX and BCL2 expression levels. Compared with normothermia, hypothermia significantly improved hind limb function; Group B achieved a higher score than Group A. Group D showed no neurologic deficiency, while the other groups showed various degrees. Group C exhibited greater neuronal apoptosis, higher BAX expression, but lower BCL2 expression than the other groups. Compared with Group A, BAX was expressed less and BCL2 more in Group B, and there was less apoptosis in Group B. Hypothermia preserves hind limb motor function and reduces neuronal death, thereby protecting rats from SCII. The spinal cord may be protected from SCII by inhibition of BAX and activation of BCL2. However, deep hypothermia may inhibit the expression of BCL2, resulting in a worse outcome than mild hypothermia.

Significance of sarcomere gene mutation in patients with dilated cardiomyopathy.

Dilated cardiomyopathy (DCM) is a myocardial disease with a high mortality rate. Approximately 40 genes have been found to be associated with DCM to date. Non-familial DCM can also be caused by gene mutations, suggesting that genetic factors were involved in the pathogenesis of DCM; therefore genetic testing is beneficial for the early diagnosis of DCM, which can facilitate the implementation of preventive measures by and within patient's families. Here, we investigated the underlying genetic mutations involved in the cause of patients with DCM. This prospective study included 240 patients with idiopathic DCM and 240 healthy volunteers. Subject clinical data were collected and polymerase chain reaction amplification was carried out on subject DNA for three candidate genes tropomyosin (TPM1), cardiac troponin T type-2 (TNNT2), and nuclear lamina protein A/C. Single nucleotide polymorphism (SNP) loci were detected in the TPM1 (rs1071646) and TNNT2 (rs3729547) genes, respectively. The genotype distributions and allele frequencies were found to satisfy Hardy-Weinberg equilibrium, which indicated that the group was representative. Statistically significant differences were found between the variant frequencies in the two SNP loci between the Kazakh patients with idiopathic DCM (IDCM) and healthy volunteers. A significant difference in the genotype distributions (P = 0.000) and allele frequencies (P = 0.000) of SNP rs1071646, and another significant difference in the genotype distributions (P = 0.000) and allele frequencies (P = 0.039) of SNP rs3729547 between Kazakhs with IDCM and Kazakh controls. These results suggest that the TPM1 (rs1071646) and TNNT2 (rs3729547) gene variants might represent risk factors for patients with DCM in the Kazakh population.

Influence of sirolimus-induced TGF-ß secretion on mouse Treg cell proliferation.

We examined the effects of co-culturing CD4+ CD25+ Treg cells with sirolimus or cyclosporin A on Treg cell proliferation and differentiation and on transforming growth factor-ß (TGF-ß) and Foxp3 expression. CD4+ CD25+ Treg cells were harvested from mononuclear cells of spleens of C57BL/6 mice using immunomagnetic beads and divided into control, sirolimus, and cyclosporine groups. Following a 96-h co-culture, Treg cells were assayed by flow cytometry. FoxP3 and TGF-ß mRNA levels and secretion were assayed by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Smad protein of the TGF-ß signaling pathway was assayed by western blot and its effect on CD4+ CD25+ FoxP3+ Treg cell proliferation was determined. Sirolimus-promoted differentiation and proliferation was examined using a TGF-ß neutralizing antibody. Sirolimus-treated CD4+ T cell TGF-ß secretion increased 2.5X over control levels (P < 0.01), but that of the cyclosporine group decreased marginally (P > 0.05). The CD4+ cell proportion decreased significantly (41.25 vs 69.22%, P < 0.01) and slightly (65.21 vs 69.22, P > 0.05) in the cyclosporine and sirolimus groups, respectively. T cell Foxp3 mRNA expression was significantly higher in the sirolimus-treated than in the cyclosporine (53.7 vs 40.2%, P < 0.05) and control groups (P < 0.01), but was significantly lower in the cyclosporine group than in controls (23.6 vs 40.2%, P < 0.01). Overall, sirolimus promoted CD4+ CD25+ Treg cell proliferation and growth in vitro, whereas cyclosporin A inhibited proliferation. Sirolimus might promote CD4+ CD25+ FoxP3+ regulatory T cell proliferation by inducing TGF-ß secretion in vivo.

Repair of cartilage defects in BMSCs via CDMP1 gene transfection.

This study aimed at investigating the ability of cartilage-derived morphogenetic protein 1 (CDMP1) gene-transfected bone marrow mesenchymal stem cells (BMSCs) loaded on the poly(lactic-co-glycolic acid) (PLGA) scaffold for the repair of laryngeal cartilage defects and make a preliminary assessment of its repair effect. The mRNA and protein expressions of hCDMP1 were detected by reverse transcriptase-polymerase chain reaction and Western blotting. The expression of type II collagen (Col II) and glycosaminoglycan (GAG) were detected by immunohistochemistry. The cytoskeletal culture systems before and after transfection were transplanted into the rabbit full-thickness defects of thyroid cartilage for observation of the repair of cartilage defects from general and histological aspects. The exogenous hCDMP1 gene could be successfully transplanted into BMSCs through adenovirus infection to obtain a stable expression. Compared with the control group, hCDMP1 gene-transfected BMSCs had enhanced secretory abilities of Col II, GAG, and other cartilage-specific matrices, with a trend of promoting cartilage differentiation. The transfected cytoskeletal complexes could more effectively repair laryngeal cartilage defects. hCDMP1 gene-transfected BMSCs/PLGA 3-D biological scaffold compounds transplanted into animal bodies could effectively repair laryngeal cartilage defects.

Expression of tyrosine hydroxylase and growth-associated protein 43 in aging atrial fibrillation patients of Xinjiang Uygur and Han nationality.

The aim of this study was to explore the changes in gene and protein expressions of tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP43) in aging atrial fibrillation patients of Xinjiang Uygur and Han nationality, and the significance of the changes. Real-time polymerase chain reaction and Western blot analysis were used to detect gene and protein expressions of TH and GAP43 in atrial tissues of 54 patients with valvular heart disease. mRNA and protein expressions of GAP43 and TH were significantly different between the sinus rhythm and atrial fibrillation groups (P < 0.05). Protein expressions of GAP43 and TH of both nationalities differed significantly between the sinus rhythm group and the atrial fibrillation group (P < 0.05), whereas there was no statistical difference between the two nationalities within each group (P > 0.05). Protein expressions of GAP43 and TH differed significantly among different age groups of different nationalities in the sinus rhythm and atrial fibrillation groups (P < 0.05); only protein expression of GAP43 differed significantly in different age groups in the atrial fibrillation group (P < 0.05). The changes of mRNA and protein expressions of TH and GAP43 played a vital role in the process of maintaining the atrial fibrillation. Therefore, increased expression of TH and GAP43 might be a molecular mechanism for left atrial myoelectricity remodeling of aging atrial fibrillation patients, which might be potential therapeutic targets of atrial fibrillation.

Effect of atorvastatin on left atrial function of patients with paroxysmal atrial fibrillation.

The aim of this study was to evaluate the effects of atorvastatin on left atrial (LA) function in paroxysmal atrial fibrillation patients. Fifty-eight paroxysmal atrial fibrillation patients were divided into two groups (treatment and control groups). The echocardiography parameters, including LA active emptying volume (LAAEV), LA active emptying fraction, LA maximum volume, LA total emptying volume, LA total emptying fraction, and LA ejection force (LAEF), were measured before treatment, and then 12 and 18 months after treatment. Compared to pre-treatment levels, the parameters reflecting LA pump function, such as LAAEV and LAEF, decreased significantly in treatment groups 12 months after treatment (P < 0.05). LAAEV and LAEF significantly increased 18 months after treatment (P < 0.05), and the indicators reflecting LA reservoir function, such as maximum volume, total emptying volume, and total emptying fraction increased significantly 18 months after treatment (P < 0.05). Compared with pre-treatment levels, LAAEV and LAEF decreased significantly 18 months after treatment in the control group (P < 0.05). These results demonstrated that long-term atorvastatin treatment could ameliorate the function of the atrium sinistrum.

A novel mutation of the MFN2 gene in a Chinese family with Charcot-Marie-Tooth disease.

Charcot-Marie-Tooth (CMT) is a group of clinically and genetically heterogeneous inherited neuromuscular disorders. At present, more than 30 loci have been reported to be associated with CMT disease; point mutations in the mitofusin 2 (MFN2) gene is one of the most common causes. We studied a Chinese family with CMT disease in which the phenotype of affected individuals varied, and the weakness condition of the distal legs in males, except the proband, was less severe than in females in this family. Linkage analysis and PCR sequencing revealed a missense mutation (NM_014874.3:c.1066 A>G) in the MFN2 gene, resulting in an animo acid substitution of threonine to alanine in condon 356 (Thr356Ala). This is a novel phenotype and mutation for CMT family.