Visceral leishmaniasis,progressive disseminated histoplasmosis and penicilliosis marneffei are infections found in both human and animals.Their clinical manefestations,morphology of the pathogens under microscope are similar.Misdiagnosis was common and prognosis was poor when wrong therapy was given.This article is to introduce the epidemiology,clinical manefestation,laboratory findings and the treatment of these infections.

Repetitive(repetitive extragenic palindromic,REP,and enterobaterial repetitive intergenic consensus,ERIC) sequences in conjunction with polymerase chain reaction technique(REP and ERIC PCR) were used to fingerprint the genomes of 27 isolates of indigenous soybean rhizobia from Xinjiang.The indigenous soybean rhizobia in Xinjiang can be clustered into relative genetic similarities of approximately 0.5,of which one group mainly includes all slow-growing rhizobia,another mainly includes all fast-growing stains. REP and ERIC PCR analysis demonstrate a substantial genetic variability within members of Xinjiang indigenous soybean rhizobial populations, which reveals that genetic similarities have certain geographical correlation, and isolates from the same site have relative higher similarities.The results show that REP and ERIC PCR analysis give effective means in genetic diversity and population structure analysis of soybean rhizobia.

Objective To observe the learning and memory changes in coal-burning type of fluorosis rats, detect the expressions of neuronal nicotinic acetylcholine receptor(nAChR) at mRNA and protein levels in rat brains and to reveal the mechanism of changed learning and memory ability. Methods Twenty-four healthy SD rats, weighting 100 - 120 g, were randomly divided into three groups(8 in each). Control group was fed with normal diet, and low- and high-dose fluoride groups were fed with corn polluted with high fluoride (fluoride were 11.30,104.20 mg/kg, respectively) during drying processes with local burning-coal from the areas of endemic fluorosis to established rat model of chronic fluorosis. After exposed to fluoride for 6 months, behavioral changes were measured by Morris water maze. Animals were sacrificed, the brain was taken, after homogenizing the fluoride content of brain tissue was determined by fluoride ion selective electrode. The α3, α4 and α7 nAChR subunits at mRNA and protein levels were analyzed by real-time PCR and Western blotting, respectively. Results For rats in low- and high-fluoride groups, the escape latency time[(12.42 ± 8.03),(17.48 ± 8.05)s] was significantly longer than that in the control[(7.04 ± 3.29)s, all P< 0.05]. For rats in high-fluoride group, the numbers of crossing the platforms (1.62 ± 0.87) and the time of staying at the platforms[(16.70 ± 5.02)s] were significantly decreased as compared to that of control[3.53 ± 1.67, (23.33 ± 5.35)s, all P < 0.05]. The fluoride content in rat brain tissue in low- or high-fluoride groups [(1.14 ± 0.04), (1.79 ± 0.04)mg/kg] was significantly higher than that of control [ (0.52 ± 0.05) mg/kg, all P < 0.05]; in addition, the amount of fluoride in brain tissue of high-fluoride group was significantly higher than that of low-fluoride group(P < 0.05). In high-fluoride group, the mRNA expressions of α3, α4 and α7 nAChR subunits in rat brains(1.51 ± 0.20,1.45 ± 0.06,1.63 ± 0.08) were significantly lower as compared to controls (1.79 ± 0.11,1.66 ± 0.14,1.83 ± 0.06, all P< 0.05); whereas there were no significant changes in mRNA levels of these receptor subunits of the rat brains between low-fluoride group(1.65 ± 0.17,1.59 ± 0.09,1.71 ± 0.03) and controls (all P > 0.05). Furthermore, the protein levels of α3, α4 and α7 nAChR subunits in rat brains of highfluoride group(0.58 ± 0.13,0.16 ± 0.03,1.41 ± 0.38) and low-fluoride group(0.56 ± 0.23,0.08 ± 0.02,0.51 ± 0.16) were significantly lower than those of controls( 1.48 ± 0.42,0.57 ± 0.21,2.56 ± 0.26, P<0.05 or < 0.01). Conclusions Decreased ability of learning and memory in coal-burning type of fluorosis rats may be associated with declined expressions of nAChR at proteins and mRNA levels, which might be the main mechanism of the behavior change.

With reverse transcriptase PCR, the transcripton of copper homeostasis relative gene Afe0329 in Acidithiobacillus ferrooxians standard strain ATCC23270 was investigated. The further analysis of genes in this transcripton was analyzed employed by Vector NTI, Blast, TMHMM Server, PSORTb software and so on. From the DNA of different strains, the transcripton of Afe0329 was amplified using special primer pairs to identify the universality of it in the genome of A.ferrooxidans strains. The results showed that gene Afe0330 and Afe0331 were cotranscribed with Afe0329, and they were in a single transcripton. Gene Afe0329 was supported to express a P1b3-type ATPase which is a heavy metal ion pumping transmembrane protein, protein AFE0330 which expressed by gene Afe0330 was a cytoplasmic protein, no significant ho- mologous sequences of Afe0330 or Afe0331 had been obtained by Blast analysis. And the transcripton of Afe0329 was universal in genome of A. ferrooxidans strains.

Reverse transcriptase-PCR experiments suggest that the two clusters of genes potentially involved in the oxidation of reduced sulfur compounds are organized as operons in strain of the acidophilic, chemolithoautotrophic bacterium Acidithiobacillus ferrooxidans ATCC 23270, the two clusters of genes including such the ORF of putative sulfate-thiosulfate-molybdate binding proteins, the ORF of putative thiosulfate: quinone oxidoreductase and the ORF of the rhodanese-like protein (P21). Bioinformatic analyses have predicted the possible promoters sequences and the possible +1 start site of transcription for the doxDA operons.

Nitrites play multiple characteristic functions in invasion and metastasis of hepatic cancer cells, but the exact mechanism is not yet known. Cancer cells can maintain the malignant characteristics via clearance of excess mitochondria by mitophagy. The purpose of this article was to determine the roles of nitrite, reactive oxygen species (ROS) and hypoxia inducing factor 1 alpha (HIF-1 α) in mitophagy of hepatic cancer cells. After exposure of human hepatocellular carcinoma SMMC-7721 cells to a serial concentrations of sodium nitrite for 24 h under normal oxygen, the maximal cell vitality was increased by 16 mg x (-1) sodium nitrite. In addition, the potentials of migration and invasion for SMMC-7721 cells were increased significantly at the same time. Furthermore, sodium nitrite exposure displayed an increase of stress fibers, lamellipodum and perinuclear mitochondrial distribution by cell staining with Actin-Tracker Green and Mito-Tracker Red, which was reversed by N-acetylcysteine (NAC, a reactive oxygen scavenger). DCFH-DA staining with fluorescent microscopy showed that the intracellular level of ROS concentration was increased by the sodium nitrite treatment. LC3 immunostaining and Western blot results showed that sodium nitrite enhanced cell autophagy flux. Under the transmission electron microscopy (TEM), more autolysosomes formed after sodium nitrite treatment and NAC could prevent autophagosome degradation. RT-PCR results indicated that the expression levels of COX I and COXIV mRNA were decreased significantly after sodium nitrite treatment. Meanwhile, laser scanning confocal microscopy showed that sodium nitrite significantly reduced mitochondrial mass detected by Mito-Tracker Green staining. The expression levels of HIF-1α, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC. Our results demonstrated that sodium nitrite (16 mg x L(-1)) increased the potentials of invasion and migration of hepatic cancer SMMC-7721 cells through induction of ROS and HIF-1α mediated mitophagy.
Acetylcysteine ; pharmacology ; Autophagy ; Carcinoma, Hepatocellular ; pathology ; Cell Line, Tumor ; Cell Movement ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Liver Neoplasms ; pathology ; Mitochondrial Degradation ; Neoplasm Invasiveness ; Nitrites ; metabolism ; Reactive Oxygen Species ; metabolism ; Sodium Nitrite ; pharmacology

Nitrites play multiple characteristic functions in invasion and metastasis of hepatic cancer cells, but the exact mechanism is not yet known. Cancer cells can maintain the malignant characteristics via clearance of excess mitochondria by mitophagy. The purpose of this article was to determine the roles of nitrite, reactive oxygen species (ROS) and hypoxia inducing factor 1 alpha (HIF-1 α) in mitophagy of hepatic cancer cells. After exposure of human hepatocellular carcinoma SMMC-7721 cells to a serial concentrations of sodium nitrite for 24 h under normal oxygen, the maximal cell vitality was increased by 16 mg x (-1) sodium nitrite. In addition, the potentials of migration and invasion for SMMC-7721 cells were increased significantly at the same time. Furthermore, sodium nitrite exposure displayed an increase of stress fibers, lamellipodum and perinuclear mitochondrial distribution by cell staining with Actin-Tracker Green and Mito-Tracker Red, which was reversed by N-acetylcysteine (NAC, a reactive oxygen scavenger). DCFH-DA staining with fluorescent microscopy showed that the intracellular level of ROS concentration was increased by the sodium nitrite treatment. LC3 immunostaining and Western blot results showed that sodium nitrite enhanced cell autophagy flux. Under the transmission electron microscopy (TEM), more autolysosomes formed after sodium nitrite treatment and NAC could prevent autophagosome degradation. RT-PCR results indicated that the expression levels of COX I and COXIV mRNA were decreased significantly after sodium nitrite treatment. Meanwhile, laser scanning confocal microscopy showed that sodium nitrite significantly reduced mitochondrial mass detected by Mito-Tracker Green staining. The expression levels of HIF-1α, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC. Our results demonstrated that sodium nitrite (16 mg x L(-1)) increased the potentials of invasion and migration of hepatic cancer SMMC-7721 cells through induction of ROS and HIF-1α mediated mitophagy.

Objective To investigate the safety and feasibility of multiple overlapping stents combined with coils in treating intracranial fusiform aneurysms, and to evaluate its therapeutic efficacy. Methods During the period from Aug. 2012 to Aug. 2013, three patients with intracranial fusiform aneurysm were admitted to authors’ hospital. The diagnosis was confirmed by CT angiography and whole cerebral angiography. Multiple overlapping stents combined with coils was carried out in all the three patients. All the patients were followed up and the clinical results were analyzed. Results Multiple overlapping stents combined with coils was successfully accomplished in all the three patients. Greater part of the aneurysmal cavity was occluded, and immediately after the procedure obvious blood whirling in the aneurysmal sac was seen. A total of 7 stents and 17 coils were used in treating the three patients. No aneurysm rupture or thrombosis occurred. The patients were followed up for 3 - 8 months. In one case the headache disappeared in 8 months, no dysneuria was detected, and angiography showed that the aneurysmal sac disappeared and the parent artery was patent. In another patient the headache disappeared in 3 months, and the angiography showed that the aneurysmal cavity had slight visualization and the parent artery was patent. The remaining patient was asymptomatic at 3-month follow-up. Conclusion For the treatment of intracranial fusiform aneurysms, multiple overlapping stents combined with coils is clinically feasible and safe with excellent short-term efficacy although its long-term results need to be further studied. (J Intervent Radiol, 2014, 23: 277-280).

A series of aralkyl-ketone-4-piperidol derivatives were synthesized and tested for their analgesic activities. All of the novel 30 compounds were prepared from 4-piperidone and alpha-halo-aralkyl-ketone through five steps, including Boc protection, nucleophilic addition in presence of CeCl3/NaI catalyst, deprotection, condensation and salification. Their structures were confirmed by 1H NMR and HRMS. Preliminary in vivo pharmacological trials showed that most of the synthesized compounds revealed analgesic effects. Among the tested compounds, 8, 13 and 22 exhibited potent analgesic activities in both mice writhing and mice hot plate model. The three compounds have low affinity for mu, delta, kappa receptors, which is a chance to find a better precursor of non-opioid analgesic for further optimization.
Analgesics, Non-Narcotic ; chemical synthesis ; chemistry ; pharmacology ; Animals ; Mice ; Molecular Structure ; Pain Measurement ; Pain Threshold ; drug effects ; Piperidones ; chemical synthesis ; chemistry ; pharmacology ; Receptors, Opioid, delta ; metabolism ; Receptors, Opioid, kappa ; metabolism ; Receptors, Opioid, mu ; metabolism ; Structure-Activity Relationship

OBJECTIVETo inquire into the relationship between lipoprotein lipase (LPL) gene D9N, N291S and S447X polymorphisms and the development of cardiovascular diseases in children with obesity.

METHODSThe polymerase chain reaction (PCR) and restriction fragment length polymorphism (RLFP) techniques were used to detect three common mutations of LPL gene exon D9N, N291S and S447X in 157 obese children and 175 normal controls. Plasma lipid and lipoprotein levels between children with different genotypes were compared.

RESULTSThe D9N and N291S gene mutations were not detected in either the obese or the control groups. There were no significant differences in the frequency of S447X gene mutation between the two groups. There were no significant differences in the levels of plasma lipid and lipoprotein between children with S447 and X447 genotypes.

CONCLUSIONSD9N and N291S gene mutations may not be risk factors associated with cardiovascular diseases in children with obesity. S447X gene mutation might not play an important role in the development of cardiovascular diseases in childhood.

Adolescent ; Cardiovascular Diseases ; etiology ; genetics ; Child ; Female ; Humans ; Lipoprotein Lipase ; genetics ; Male ; Mutation ; Obesity ; genetics ; Risk Factors