Aquaporin-11 containing a divergent NPA motif has normal water channel activity

Recently, two novel mammalian aquaporins (AQPs), AQPs 11 and 12, have been identified and classified as members of a new AQP subfamily, the “subcellular AQPs”. In members of this subfamily one of the two asparagine-proline-alanine (NPA) motifs, which play a crucial role in selective water conduction, are not completely conserved. Mouse AQP11 (mAQP11) was expressed in Sf9 cells and purified using the detergent Fos-choline 10. The protein was reconstituted into liposomes, which were used for water conduction studies with a stopped-flow device. Single water permeability (pf) of AQP11 was measured to be 1.72 ± 0.03 × 10^− 13 cm³/s, suggesting that other members of the subfamily with incompletely conserved NPA motifs may also function as water channels.     

Involvement of aquaporins in a mouse model of rotavirus diarrhea

Rotavirus diarrhea is a major worldwide cause of infantile gastroenteritis; however, the mechanism responsible for intestinal fluid loss remains unclear. Water transfer across the intestinal epithelial membrane seems to occur because of aquaporins（AQPs）. Accumulating evidence indicates that alterations in AQPs may play an important role in pathogenesis. Here, we focus on changes in AQPs in a mouse model of rotavirus diarrhea. In the present study, 32 of 35 mice developed diarrhea and mild dehydration within 24 hours after infection with rotavirus strain SA11. Intestinal epithelial cells demonstrated cytoplasmic vacuolation, malaligned villi, and atrophy. AQP1 expression was significantly attenuated in the ileum and colon in comparison with controls; likewise, AQP4 and-8 protein expression were significantly decreased in the colon of rotavirus diarrhea-infected mice. In contrast, AQP3 protein expression was significantly increased in the colon of rotavirus-infected mice in comparison with controls. These results indicate that rotavirus diarrhea is associated with the downregulation of AQP1,-4, and-8 expression. Therefore, AQPs play an important role in rotavirus diarrhea.     

Insight into hypoxic preconditioning and ischemic injury through determination of nPKCε-interacting proteins in mouse brain

Cerebral hypoxic preconditioning (HPC) provides neuroprotection by intracellular signaling pathways. We previously demonstrated that novel protein kinase Cε (nPKCε) activation participated in cerebral HPC development. In this study, we explore the role of nPKCε in HPC-induced neuroprotection against middle cerebral artery occlusion (MCAO)-induced ischemic injury and identify its possible signaling molecules. A total of 131 adult male BALB/c mice were divided into eight groups: normoxic control (n = 9), HPC (n = 9), HPC + εV1–2 (n = 13), Sham (n = 19), HPC + sham (n = 6), Ischemia (I, 6 h MCAO, n = 31), HPC + I (n = 25) and HPC + εV1–2 + I (n = 19). nPKCε specific inhibitor εV1–2 was administered via intracerebroventricular injection. Western blot, 2,3,5-triphenyltetrazolium chloride staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were applied to determine nPKCε membrane translocation, infarction volume and programmed cell death (PCD), respectively. Two-dimensional gel electrophoresis (2-De) and matrix assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) were used to identify nPKCε-interacting proteins, followed by bioinformatics analysis of genee ontology (GO) to predict nPKCε-specific signaling pathways. Our results showed that HPC attenuates MCAO-induced brain injuries and stabilized nPKCεmembrane translocation in peri-infarct region, which was abolished by nPKCε-speecific inhibitor εV1–2. Proteomics analysis revealed 8 up- and 3 down-regulated nPKCε-interacting proteins both in cytosolic and particulate fractions of HPC mouse brain. GO analysis predicted 25 significant nPKCε-specific signaling pathways among the 16 identified nPKCε-interacting proteins in brain of HPC mice. This study is the first to report multiple nPKCε-interacting proteins and their signaling pathways in HPC mouse brain, suggesting that nPKCε signaling molecules is responsible for HPC-induced neuroprotection against cerebral ischemic injuries of mice.     

Cholecalciferol (vitamin D 3) improves cognitive dysfunction and reduces inflammation in a rat fatty liver model of metabolic syndrome

Aim

The aim of this study was to examine the effects of cholecalciferol on systemic inflammation and memory in the setting of fatty liver disease in rats.

Materials and methods

To induce the development of fatty liver disease, the rats were fed a 35% fructose solution over 8 weeks. Group I (n = 6) was designated as the control group and fed with standard rat chow. Group II (n = 6) was provided with, standard rat chow, and 0.3 μg/kg/day of oral cholecalciferol over a duration of 2 weeks. In addition to standard rat chow, group III (n = 6) and group IV (n = 6) were given 4 mL of the 35% fructose solution per day via oral gavage for 8 weeks. However, group IV was also given 0.3 μg/kg/day of oral cholecalciferol over 2 weeks. After the treatment period, passive avoidance tasks were performed by all groups. The liver and brain were harvested for subsequent biochemical and histopathologic analyses.

Key findings

The development of fatty liver extends the memory latency period of passively avoiding tasks after 1 trial. Moreover, there were increases in brain TNF-α and plasma MDA levels according to two-way analysis of variance. Cholecalciferol supplementation decreased the latency period of passively avoiding tasks in rats with hepatosteatosis, and also significantly reduced brain TNF-α and plasma MDA levels.

Significance

Fatty liver may contribute to the development of systemic inflammation, which affects cognition and causes deficits in memory; however, the anti-inflammatory and antioxidant properties of vitamin D may improve the cognitive function of rats with hepatosteatosis.     

Expression,localization and possible functions of aquaporins 3 and 8 in rat digestive system

Although aquaporins (AQPs) play important roles in transcellular water movement, their precise quantification and localization remains controversial. We investigated expression levels and localizations of AQP3 and AQP8 and their possible functions in the rat digestive system using real-time polymerase chain reactions, western blot analysis and immunohistochemistry. We investigated the expression levels and localizations of AQP3 and AQP8 in esophagus, forestomach, glandular stomach, duodenum, jejunum, ileum, proximal and distal colon, and liver. AQP3 was expressed in the basolateral membranes of stratified epithelia (esophagus and forestomach) and simple columnar epithelia (glandular stomach, ileum, and proximal and distal colon). Expression was particularly abundant in the esophagus, and proximal and distal colon. AQP8 was found in the subapical compartment of columnar epithelial cells of the jejunum, ileum, proximal colon and liver; the most intense staining occurred in the jejunum. Our results suggest that AQP3 and AQP8 play significant roles in intestinal function and/or fluid homeostasis and may be an important subject for future investigation of disorders that involve disruption of intestinal fluid homeostasis, such as inflammatory bowel disease and irritable bowel syndrome.     

Structural evaluation of the effects of chronic ethanol ingestion on the testis of Calomys callosus

Chronic exposure to ethanol may results in pathophysiologic changes in cellular function. The present work was designed to investigate the morphology of testis submitted to experimental ethanol ingestion. Experimental animals were divided into two groups. The control group (n = 23) received a solid diet and tap water and the alcoholic group (n = 23) received the same solid diet and ethanol P.A. diluted 20% in water (v/v). After 120 days of treatment, all animals were anesthetized, weighed and sacrificed. Testosterone and luteinizing hormone levels in serum were lower in the alcoholic group than in the control group. Histological and ultrastructural alterations were observed in the testicular alcoholic germinative cells like enormous spaces, lipid droplets accumulation, digestive vacuoles, irregular diameter of the seminiferous tubules and interstitial dilated blood vessels. It was concluded that 20% ethanol provokes lesions on the testis germinative epithelium probably inducing gonadal dysfunction.     

Prolonged Ethanol Ingestion Increases Renal AQP2 and AQP3 Expression in Adult Ratsand in Their Offspring

This study evaluates the effect of prolonged ethanol ingestion on the renal ability to concentrate urine. Suckling Wistar rats born to mothers given ethanol before and during gestation and suckling periods (ethanol-exposed offspring) were used and the results were compared with those obtained from offspring of dams given diets containing no ethanol. Comparisons were also made between progenitors with or without prolonged ethanol ingestion. Body and kidney weights; arginine-vasopressin (AVP) and aldosterone plasma levels; plasma, urine and renal papillary osmolality; urine outflow; kidney AQP2, AQP3 and AQP4 expression and diencephalon AVP mRNA expression were determined. As compared with control offspring, the ethanol-exposed offspring present i) lower body and kidney weights; ii) lower urine outflow; iii) higher renal AQP2 and AQP3 mRNA; iv) higher renal AQP2 protein content and v) higher urine and renal papillary osmolality. These changes were also observed in the ethanol-treated progenitors, although they were of smaller magnitude. Plasma osmolality, renal AQP4 mRNA, AVP plasma levels and diencephalon AVP mRNA expression were not affected by the ethanol treatment. Plasma levels of aldosterone were only significantly increased in the ethanol-exposed suckling rats. It is concluded that maternal ethanol ingestion before and during gestation and suckling periods affects the renal function of the offspring, up-regulating renal AQP2 expression by an AVP-independent mechanism. Ethanol-treated progenitors manifest similar renal changes, although of lesser magnitude than the offspring.     

Numerical defects in CD8CD28 T-suppressor lymphocyte population in patients with type 1 diabetes mellitus and multiple sclerosis

Type 1 diabetes mellitus (T1D) and multiple sclerosis (MS) are organ-specific autoimmune diseases leading to an attack of auto-aggressive lymphocytes against the pancreatic β-cells and central nervous system, respectively. Using four-colour flow cytometry, T-lymphocyte populations having an important function in autoimmune processes were analyzed. T-regulatory cells (Treg) CD4⁺CD25⁺CD127^low, T-suppressor cells (Ts) CD8⁺CD28⁻, activated helper CD4⁺CD25⁺CD127⁺ and cytotoxic CD8⁺CD25⁺ T-cells and also naive CD4⁺CD45RA⁺ and memory T-cells CD4⁺CD45RO⁺ were compared in the group of patients with T1D (n = 30), MS (n = 31) and in the group of healthy controls (n = 29). Significant differences in Ts cells, activated helper and cytotoxic cells and also memory T-cells were recognized in the group of T1D patients compared to healthy controls. Ts population was significantly lowered in MS patients as well. However, no significant differences were noticed in Treg population. The observed data demonstrate significant differences among patients with T1D and MS in comparison to healthy individuals.     

Expression of basic fibroblast growth factor,protein kinase C and members of the apoptotic pathway in skeletal muscle of streptozotocin-induced diabetic rats

This study investigated the potential mechanisms that may underlie diabetes induced amyoatrophy. Sprague-Dawley rats were either injected intraperiotneally with STZ (test group; N = 8) to induce diabetic-like symptoms (blood glucose level ≥16.65 mmol/L) or with buffer (control group; N = 8). Differences in muscle structure between the STZ-induced diabetic and control groups were evaluated by histochemistry. Protein and mRNA levels of basic FGF (bFGF), bax, bcl-2, and caspase 3 in skeletal muscle were compared between the 2 groups using immunohistochemistry and quantitative PCR, respectively. Serum level of insulin and protein kinase C (PKC) were measured by competitive RIA and ELISA, respectively. Unlike control animals, the skeletal muscle fibers from STZ-induced diabetic animals were broken and pyknotic, the sarcomeric structure disrupted, and mild hyperplasia of interstitial adipose tissues was detected. The serum level of PKC was higher (P = 0.003) and the protein and mRNA levels of bFGF in skeletal muscle were lower (P = 0.001) in STZ-induced diabetic versus control animals. Protein and mRNA levels of the apoptosis promoting genes caspase-3 and bax were higher in skeletal muscle from STZ-induced diabetic rats as compared to control animals (P < 0.001 and P = 0.037, respectively), while mRNA and protein levels of bcl-2, an inhibitor of apoptosis, was lower in STZ-induced diabetic rats versus control animals (P = 0.026). Increasing apoptosis in skeletal muscle from STZ-induced diabetic rats was further demonstrated by TNNEL assay. Our findings suggest that enhanced PKC levels, reduction of bFGF expression, and increased in apoptosis might be associated with the development of diabetes-induced myoatrophy.     

3种模拟中医体征的体虚便秘大鼠模型建立及效果观察

目的：分别建立大鼠血虚、阴虚和阳虚便秘模型并比较其结肠动力、结肠水代谢、结肠黏液分泌和结肠水通道蛋白2（AQP2）的表达水平。方法：40只SD大鼠,雌雄各半,随机分为4组（n=10）：正常对照组（N）、血虚便秘组（XC）、阴虚便秘组（YC）、阳虚便秘组（YAC）。分别采用放血+洛哌丁胺、甲状腺素+洛哌丁胺、冰水刺激+洛哌丁胺建立血虚便秘、阴虚便秘、阳虚便秘大鼠模型,放血每周1次,药物每天灌胃1次,连续42 d。检测大鼠活动状态、体质量、大便性状、口肛传输时间、小肠推进率、粪便和结肠含水量等体征指标,对结肠组织进行AB-PAS染色和免疫组化染色,观察黏液分泌情况和AQP2表达水平。结果：与正常对照组比较,3种模型大鼠体重增长减慢;造模第40天自主活动量变化率由大到小依次为YC、XC和YAC;造模第30天出现固体硬质粪便,粪便评分升高顺序为XC、YC和YAC;口肛传输时间均显著延长、小肠推进率均显著降低（P < 0.05,P < 0.01）,肠动力减低顺序为YC、YAC和XC;粪便含水量均显著减少（P < 0.05,P < 0.01）,XC和YAC组大鼠结肠含水量显著减少（P < 0.05,P <0.01）,YC大鼠结肠含水量有减少趋势,结肠水代谢顺序为YC、YAC和XC;3种模型大鼠结肠黏膜层腺管和杯状细胞出现不同程度缩小,黏液分泌减少,分泌功能障碍顺序为YAC、YC和XC,且近端和远端结肠AQP2的表达均显著增加（P < 0.05,P < 0.01）,增加顺序近端结肠为YAC、YC、XC,远端结肠为YAC、XC和YC。结论：复合因素长期刺激均可建立符合中医体征的便秘大鼠模型,且各模型大鼠结肠运动、结肠水代谢、结肠黏液分泌和AQP2表达水平存在一定的差异。     

Undernutrition during foetal to prepubertal life affects aquaporin 9 but not aquaporins 1 and 2 expression in the male genital tract of adult rats

Expression of aquaporin water channels (AQPs) in the male excurrent ducts, is of major importance for local water movements. To study the influence of pre- and postnatal undernutrition on AQP-expression in the adult male genital tract, 4 pregnant female rats were fed ad libitum (control group) and 4 with 33.5% of gestational feed requirements (underfed group). Feeding restriction of underfed group pups continued up to weaning (25 days of age), then all pups were fed ad libitum until slaughtered at 100 days of age. Epididymides were sampled and processed for aquaporin immunohistochemistry. Expression of AQP1 was similar either in the control and underfed groups of rats, strongly evidenced at the apical and lateral plasma membrane of the efferent ducts non-ciliated cells, in the smooth muscle cells surrounding epididymal duct and in blood vessel endothelium throughout the epididymis. AQP2-immunoreactivity was present in the corpus and cauda regions, strongly expressed in the principal cells of both groups of rats. In contrast, AQP9 expression was modified by early life undernourishment, as it was weakly evidenced at the microvilli in the principal cells and strongly diminished or completely lacked in the clear cells of the cauda, in underfed group epididymides. Since it is known that clear cells are involved in luminal fluid acidification, this function might be altered in adult animals, which were underfed during early life.     

Investigate of AQP gene expression in the liver of mice after ischemia–reperfusion

Ischemia–reperfusion (IR) injury usually occurs during liver transplantation. Aquaporins (AQPs) are transmembrane channels that facilitate water permeability through cell membranes and are essential for the regulation of water homeostasis. Changes in the AQPs expression have been correlated with several inflammatory diseases. Less is known about AQPs expression in hepatic ischemia reperfusion injury. To clarify the roles of AQPs in IR injury, in this current study we examined the gene expression patterns of AQP1, 8 and 9 in the liver after IR injury. Male balb/c mice were exposed to partial (70%) hepatic ischemia for 65 min and then randomized into five groups of reperfusion [0 h (A), 8 h (B), 1 day (C), 3 days (D), and 7 days (E)]. A surgical group was also selected as the sham group. Serum and liver tissue samples were collected for evaluation of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and liver histopathology. Real time PCR was performed to evaluate the AQPs expression. I/R injury resulted in a significant increase in ALT and AST (p?<?0.05) compared to sham mice in each group. The gene expression of AQPs was significantly increased in the IR group compared with the sham group (p?<?0.05). AQP8 and AQP1 after 8 h (group B) showed the highest gene expression in comparison with other groups, but the highest level of AQP9 gene expression was observed after 1 day (group C). Pathologic changes in the liver after reperfusion were confirmed the IR. In the IR group cytoplasmic vacuolization, inflammatory cell infiltration and focal necrosis were detected. In conclusion, our findings indicated that the damage caused by ischemia–reperfusion in the liver can change the expression of AQP genes, which can interfere with hepatocellular homeostasis and their function. Upregulation of AQP1, 8 and 9 could contribute to the development of hepatocellular swelling after hepatic IR injury.     

Influence of inflammatory response,infection, and pulmonary function in cystic fibrosis

Aims

Recurrent infections and activation of the inflammatory response affect the prognosis of cystic fibrosis (CF). We investigated the relationship between inflammatory response, infection, and pulmonary function in CF.

Main methods

A clinical-cross-sectional study was conducted with 86 subjects: control group (CG, n = 31, the same age and sex of the CF group), and CF group (CFG, n = 55, age: 1–16 years), further distributed into CFG negative or positive bacteriology (CFGB⁻/CFGB⁺), and CFG negative or positive Pseudomonas aeruginosa (CFGPa⁻/CFGPa⁺). Using the Wald test, multiple linear regression (95% confidence interval) was performed between CG and CFG, and between CG and each of the CF subgroups (CFGB⁻/CFGB⁺ and CFGPa⁻/CFGPa⁺). The inflammatory markers evaluated were myeloperoxidase (MPO), adenosine deaminase (ADA) activities, interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNF-α), C-reactive protein (CRP), nitric oxide metabolites (NOx) levels, and total and differential leukocyte counts.

Key findings

After adjusting for sex and age, CFG compared to CG revealed an increase of MPO, IL-1β (P < 0.001 in all subgroups), and CRP: CFG (P = 0.002), CFGB⁻ (P = 0.007), CFGB⁺ (P = 0.009), CFGPa⁻ (P = 0.004) and CFGPa⁺ (P = 0.020). NOx (P = 0.001, P < 0.001), leukocytes (P = 0.002, P = 0.001), and neutrophils (P = 0.003, P < 0.001) were increased in CFGB⁺ and CFGPa⁺, respectively. A negative correlation between FEV₁ and leukocytes (P = 0.008) and FEV₁ and neutrophils (P = 0.031) resulted in CFG.

Significance

The inflammatory response characterized by the increase of MPO, IL-1β, and CRP is determinant for CF. Also leukocytosis due to neutrophilia determines the pulmonary function deficiency in this disease.     

Ionic metallomesogens derived from silver(I) bis-amine complexes: Structure and mesogenic behavior

Complexes [Ag(NH₂R)₂]X, (X = NO₃, R = -C₆H₄-C_nH_2n+1-p, -C₆H₄-O-C_nH_2n+1-p, -CH₂-C₆H₄-O-C_nH_2n+1-p, n = 6, 8, 10, 12, 14; X = BF₄, R = -CH₂-C₆H₄-O-C_nH_2n+1-p, n = 6, 8, 10, 12, 14; X = OAc, R = -CH₂-C₆H₄-O-C₁₀H₂₁-p; X = CF₃SO₃, R = -CH₂-C₆H₄-O-C₁₀H₂₁-p) have been prepared. They all show S_A mesophases corresponding to two kinds of structures, already present in the solid state. The alkylaniline and alkoxyaniline derivatives adopt a bilayered structure where the cation has an extended centrosymmetric conformation. The benzylamine derivatives contain U-shaped cations giving rise to a bilayered structure which allows microsegregation of the organic part of the molecule from the inorganic Ag?(anion) part. Some degree of interdigitation of the terminal chains is observed for all the complexes with aryl containing ligands.     

Eimeria tenella: utilization of a nasal vaccine with sporozoite antigens incorporated into Iscom as protection for broiler breeders against a homologous challenge

The aim of this study was to evaluate a nasal vaccine using antigens derived from sporozoites of Eimeria tenella incorporated into Iscom to protect broiler chicks. Forty-five one-day-old chickens (Cobb), unvaccinated against coccidiosis, were used in this experiment. The birds were maintained in separated battery cages and divided into three groups: G1 (n = 15), G2 (n = 15), and G3 (n = 15). G1 received 50 μg of sporozoites + Iscom vaccine, G2 received Iscom without antigens, and G3 received only PBS. The treatments were administered by nasal route on days 0, 7, and 21 of the experiment. On the 28th day, all birds were challenged with 105 sporulated oocysts of E. tenella. On the challenge day, three birds from each group were euthanized to evaluate lymphocyte proliferation. Lesion scores were obtained from five birds from each group, 7 days after challenge. The remaining animals were euthanized on the 50th day. The mean lymphocyte proliferation responses were significantly different (P = 0.03); G1 was 2.3-2.6 times more elevated than G2, and G3 (P < 0.001). 83% of the birds from G1 showed an IgY antibody reaction by ELISA at challenge. The means for oocysts shedding were 16,890 ± 20,511, 48,080 ± 50,047, and 65,020 ± 74,461, for G1, G2 and G3 birds, respectively. There was no significant difference (P > 0.17) in oocysts shedding between groups. However, the G1 and G2 chicks demonstrated reduction in percentage of oocyst shedding when compared to control birds (G3) by 74.02% and 26.05%, respectively. The average lesion scores were G1 = 0.4, G2 = 1, and G3 = 2. This study demonstrated that the lowest lesion score and oocyst shedding were observed in the birds from the group that received antigens derived from sporozoite with an Iscom adjuvant (G1). These results suggest that this vaccine can induce protection against avian coccidiosis.     

Enhanced expression of human β-defensin 2 in peripheral lungs of patients with chronic obstructive pulmonary disease

Human β-defensin 2 (hBD-2) has antimicrobial activity and may play a role in airway mucosal defense, but studies have not yet examined its expression in lung tissue of patients with chronic obstructive pulmonary disease (COPD). Here we investigated hBD-2 levels in lung tissues of COPD patients and analyzed their correlations with IL-8, IL-1β, cigarette smoking and lung function in order to see whether the protein may be involved in pathogenesis of the disease. Peripheral lung tissue specimens were obtained from 51 patients who underwent lung resection for peripheral lung cancer: healthy non-smokers (n = 8), healthy current smokers (n = 7), non-smokers with COPD (n = 11), and current smokers with COPD (n = 25). RT-PCR and immunohistochemical staining were used to detect expression levels of hBD-2, IL-8 and IL-1β. Expression of hBD-2 mRNA was significantly higher in COPD patients than in healthy controls, and significantly higher in current smokers than in non-smokers (p < 0.05). Among healthy controls, hBD-2 mRNA levels were similar between current smokers and non-smokers. Immunohistochemistry showed hBD-2 protein to be expressed mainly in epithelia of distal bronchioles and its expression pattern among our patient groups mirrored that of the mRNA. IL-8 mRNA levels were significantly higher in COPD patients than in healthy controls (p < 0.05), while IL-1β mRNA levels did not differ significantly among the groups. Levels of hBD-2 mRNA positively correlated with levels of IL-8 mRNA (r = 0.545, p = 0.002), and negatively correlated with FEV1/FVC ratios and with predicted FEV1% values (r = −0.406, p = 0.011). Our results indicate that hBD-2 expression is elevated in distal airways of COPD patients and that it may be involved in pathogenesis of the disease. Our data implicate cigarette smoking as a factor that may elevate hBD-2 levels in lung tissues of COPD patients.     

Reduced expression of aquaporin 9 in tubal ectopic pregnancy

Previous studies demonstrate significant roles for passive water channels (aquaporins, AQPs) in maintaining water homeostasis in cell membranes of endometrial cells during decidualisation and embryo implantation. However, there is little information regarding the role of AQPs in the human fallopian tube, specifically their role in human tubal ectopic pregnancy. In this study we took tissue samples from the site of implantation of tubal ectopic pregnancy (group 1, N = 30, mean age 32 years, range 23–42) and the corresponding non-implantation site in women undergoing salpingectomy for tubal pregnancy (group 2). Ampullary fallopian tubes during mid-secretory phase were collected as control group (group 3, N = 17, mean age 37 years, range 30–50). Thin sections were prepared and stained with anti-AQP9, and, for estrogen and progesterone receptors in each group. Immunohistochemical studies showed that AQP9 proteins localize in the cytoplasm of epithelial cells of Fallopian tube. Expression of AQP9 was significantly reduced during tubal pregnancy compared to controls (group 1 vs. group 3, P = 0.036; group 2 vs. group 3, P = 0.029), and, this reduced expression was not related to estrogen receptor or progesterone receptor status (group 2, ER vs. AQP9, Pearson r = 0.173, P = 0.361; PR vs. AQP9, Pearson r = 0.124, P = 0.514, respectively). Similarly, there is no correlation between AQP9 and estrogen receptor or progesterone receptor status in the normal group (group 3, ER vs. AQP9, Pearson r = ?0.026, P = 0.923; PR vs. AQP9, Pearson r = ?0.292, P = 0.255, respectively). Reduced expression of AQP9 in human fallopian tube may contribute to aspects of pathophysiology of tubal ectopic pregnancy.     

Increased Expression of AQP 1 and AQP 5 in Rat Lungs Ventilated with Low Tidal Volume is Time Dependent

Background and Goals

Mechanical ventilation (MV) can induce or worsen pulmonary oedema. Aquaporins (AQPs) facilitate the selective and rapid bi-directional movement of water. Their role in the development and resolution of pulmonary oedema is controversial. Our objectives are to determine if prolonged MV causes lung oedema and changes in the expression of AQP 1 and AQP 5 in rats.

Methods

25 male Wistar rats were subjected to MV with a tidal volume of 10 ml/kg, during 2 hours (n = 12) and 4 hours (n = 13). Degree of oedema was compared with a group of non-ventilated rats (n = 5). The expression of AQP 1 and AQP 5 were determined by western immunoblotting, measuring the amount of mRNA (previously amplified by RT-PCR) and immunohistochemical staining of AQPs 1 and 5 in lung samples from all groups.

Results

Lung oedema and alveolar-capillary membrane permeability did not change during MV. AQP-5 steady state levels in the western blot were increased (p<0.01) at 2 h and 4 h of MV. But in AQP-1 expression these differences were not found. However, the amount of mRNA for AQP-1 was increased at 2 h and 4 h of MV; and for AQP 5 at 4 h of MV. These findings were corroborated by representative immunohistochemical lung samples.

Conclusion

In lungs from rats ventilated with a low tidal volume the expression of AQP 5 increases gradually with MV duration, but does not cause pulmonary oedema or changes in lung permeability. AQPs may have a protective effect against the oedema induced by MV.     

Transition metal halide salts of 8-methylquinolinium: Synthesis and structures of (8-methylquinolinium)2 MX4·nH2O (M = Cu, Co, Zn; X = Cl, Br; n = 0, 1)

The reactions of metal(II) chlorides and bromides with 8-methylquinoline (8-mequin) in neutral and acidic solutions were investigated. The reaction with ZnCl₂, ZnBr₂, CoCl₂, CoBr₂, CuCl₂ or CuBr₂ with the appropriate HX in water or aqueous ethanol gave complexes of the formula (8-mequin)₂MX₄ (1, M = Cu, X = Cl; 2, M = Cu, X = Br; 3, M = Co, X = Cl; 4, M = Co, X = Br) or (8-mequin)₂ZnX₄·nH₂O (5, X = Cl, n = 0; 6, X = Br, n = 0; 7, X = Cl, n = 1; 8, X = Br, n = 1). Crystals of 1, 2 and 4-8 suitable for single crystal X-ray diffraction were obtained and the structures reported. Compounds 1 and 2 crystallize in the monoclinic space group C2/c, while 4-8 crystallize in the triclinic space group, . Variable temperature magnetic susceptibility data indicate very weak interactions for the copper compounds 1 and 2, while the magnetic behavior of 3 and 4 is dominated by single ion anisotropy, with weaker antiferromagnetic interactions.     

Structure and luminescence of copper(I) cyanide-amine and -sulfide networks

Copper(I) cyanide reacts with various liquid amines and sulfides (L) under solvent-less conditions to form (CuCN)L_n, n = 0.5, 0.57, 0.75, 0.8, 1, 1.25, 1.5, 2. New X-ray structures are reported for L = Py (Py = pyridine, n = 0.57), 2-MePy (n = 1), 3-EtPy (n = 1.5), 2-ClPy (n = 1), 3-ClPy (n = 2), 3-MeOPy (n = 2), 4-^tBuPy (n = 1.5), piperidine (n = 1.25), N-methylmorpholine (n = 1), N,N-dimethylcyclohexylamine (n = 1), 1-methylimidazole (n = 3), Me₂S (n = 1), and tetrahydrothiophene (n = 1). The amine structures (except for the monomeric 1-methylimidazole complex) reveal 1D CuCN chains decorated with 0-2 L per metal atom. Chain structures observed include zigzag, helical and figure-8 helical. The CuCN-sulfide structures show sulfur-bridging of CuCN chains. In some cases (CuCN)L_?1.5 species are transformed to (CuCN)L under vacuum. Thermal analysis shows facile release of ligand, yielding CuCN. Most of the (CuCN)L_n products are photoluminescent, emitting in the visible region. In some cases, coordination of very similar amines results in remarkably different emission spectra.