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A hundred and ninety one representative brown rice samples from the Chinese Rice Genebank and the DH population derived from the cross of japonica upland rice IRAT109 with paddy rice Yuefu were selected for this study. Their protein content range was 5.90%-14.50%. Near-infrared diffusive spectroscopy (NIDRS) and partial least square (PLS) were used to determine protein content with different wavelength ranges and data preprocessing methods for regression and information extraction. The object function [R/(1+RMSECV)] of quantitative model was defined, and the samples of calibration and validation tests were classified by projective distribution of PLS loadings. These methods were applied to the optimization of the calibration model. It is demonstrated that the calibration model developed by the spectral data pretreatment of the first derivative + standard vector normalization with the same spectral region (5 000-9 000 cm(-1) resulted in the best determination of protein content in brown rice when the maximum values of the object function were reached. The maximum values of the object functions of calibration and validation sets were 0.701 and 0.687, respectively. Projective distributions of PLS loadings were used to validate the models, and the result was the same as that of validating model by object function [R/(1+RMSECV)].

Dear Editors,Tian and colleagues summarized the role of Th22 cells and IL-22 in inflammatory and autoimmune diseases [1]. Their review was well written, whereas it might be strengthened by suppleme...

In this paper, allelic variation and genetic diversity among geographies and growth habit types were studied by using 223 accessions of common wild rice primary core collection in Guangxi Province, with 34 SSR primers locating on 12 chromosomes of rice and 19 phenotypic traits. In the results, 24.91 alleles were detected per locus on average with a range from 7 to 48. Compared to the cultivated rice, the wild rice showed more allelic variations. The ratio of heterozygote of SSR locus was 32.01% on average, and it's range was 1.35% 81.31%. The frequency of heterozygote of SSR locus in Oryza rufipogon Griff was much higher than in Oryza sativa L. The geographical distribution of genetic diversity measured by SSR markers was not completely accordant with that by phenotypic traits. At DNA level, more wild rice individuals and higher genetic diversity were included within the area covering north latitude 22 degrees - 23 degrees and 23 degrees - 24 degrees (comprising Longan, Fusui, Yongning, Xiangzhou, Laibin, Xuanwu, Yulin and Guigang county), which formed the center of genetic diversity. But the center of genetic diversity at the phenotypic level located within north latitude 21 degrees - 22 degrees and 22 degrees - 23 degrees. Among the four growth habit types, the genetic diversity from high to low was found respectively in prostrate type, sloping type, slighting type, and erect type at both DNA and phenotypic levels.

A DH (doubled haploid) population derived from a cross between Japonica upland rice IRAT109 and Japonica paddy rice Yuefu,was used in this study. Three culm traits, basal culm thickness(BCT), culm length (CL) and culm strength (CS), of DH lines and their parents under upland and lowland ecosystems at milk stage were studied. There were very significant positive correlations between BCT and CL, between BCT and CS and between CL and CS. Data from upland and lowland ecosystems were analyzed respectively and jointly, based on a constructed molecular linkage map(including 94 RFLP markers and 71 SSR markers and covering 1 535. 1cM)and the software QTLmapper version 1.0. A total of nine additive QTLs and five pairs of epistatic QTLs associated with BCT, CL, and CS were found by data analysis respectively. Six additive QTLs and six pairs of epistatic QTLs associated with BCT and CL were detected by data analysis jointly. Six additive QTLs and one pair of epistatic QTLs were detected by both methods. Two additive QTLs and two pairs of epistatic QTLs ( bct1a, c/9, c/6a-c/6c and cs5-cs12) for culm traits with general contributions of over 30% to phenotypic variation might be useful for upland rice lodging resistance molecular breeding under upland ecosystem.

Using histochemistry and optical microscope, we examined the number and the size of amyloplasts in specialized tissues of gravitropically receptive organs-tissues such as the coleoptile and sheath of rice mutant (insensitive to gravity) and wide type (Oryza sativa L. subsp. japonica) (Zhonghua 11). We found there was no statistical difference between the mutant and wide type, both of which grew on earth or on the clinostat respectively. On earth, it was found that amyloplasts sedimented at the distal end of each cell of the special starch sheath tissues and re-sedimentation of amyloplasts toward the direction of gravity was almost completed in 5 minutes after inverting the seedlings. On the clinostat, amyloplasts dispersed in the starch sheath tissue. Such observations indicated that the mutation was not resulted from the starch-deficiency or starch-absence, the further research is going on.

Fuentes and colleagues described a case with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis suspected to be complicated by posterior reversible encephalopathy syndrome (PRES) [1]. This adds to the accumulating evidence that PRES may be associated with ANCA-associated vasculitis. However, we have some concern about the diagnosis of this case. PRES (also termed reversible posterior leukoencephalopathy syndrome, RPLS) represents a clinical and radiological syndrome characterised by reversible vasogenic oedema [2] in the posterior brain, which primarily arises from autoregulation failure and endothelial dysfunction [3]. The reversible vasogenic oedema, as most specifically and sensitively detected by apparent diffusion coefficient (ADC) map of diffusion-weighted imaging (DWI), preferably involving posterior white matter, and typical clinical manifestations like acute onset of headache, confusion or decreased level of consciousness, visual disturbance and seizures can help to diagnose a typical PRES. Although lesions might be revealed by T2-weighed imaging (T2WI) or fluid attenuated inversion recovery images (FLAIR) of magnetic resonance imaging (MRI), they are not specific for vasogenic oedema [4]. Atypical cases are not rare [3], whereas they should be diagnosed with caution, especially after rigid exclusion of other confounding disorders. Differential diagnoses of PRES include metabolic encephalopathy, inflammatory demyelinating diseases, vasculitis, etc. Connective-tissue diseases, including systemic lupus erythematosus (SLE), polyarteritis nodosa, Wegener’s granulomatosis, microscopic polyangiitis, Henoch Schonlein purpura, Takayasu’s arteritis and thrombotic thrombocytopenic purpura, have been suggested as disorders in which PRES can develop [1, 5–7]. The central nervous system (CNS) complications in connective-tissue diseases are not uncommon, which include vasculitis [8], acute or subacute infarction [9] and PRES [1, 5–7]. Demyelination, inflammatory lesions, ischaemia or oedema may present as reversible changes in the brain as revealed by neuroimaging modalities. Therefore, reversibility, not only clinical but radiological, and vasogenic oedema as detected by ADC map of DWI, as well as well-established risk factors predisposing to hypertension, such as phaeochromocytoma, glomerulonephritis, eclampsia and receiving cytotoxic and immunosuppressant drugs [3], should be confirmed by clinical and neuroimaging examinations to diagnose this case as a typical PRES. In summary, PRES represents a clinicoradiological syndrome, the diagnosis of which relies on typical clinical and neuroimaging findings.

Ann Saudi Med 2014 September-October www.annsaudimed.net 1 Symmetric thalamic lesions may appear in various disorders, such as in acute disseminated encephalomyelitis, acute hemorrhagic leukoencephalitis, severe hypoxia or traumatic injury, toxins, inflammation, tumors, metabolic disorders, acute necrotizing encephalopathy, arterial or venous infarct, and so on.1-3 Bilateral thalamic lesions occasionally result from venous occlusion, especially thrombosis of the deep cerebral veins (eg, vein of Galen and straight sinus).4 Additionally, as the management and prognosis were distinct between patients with venous and arterial occlusion, early diagnosis is of great importance.5,6 MRI of the patient showed bilateral thalamic lesions with features of abnormal signal intensity, as follows: the T1-weighted image (T1WI) decreased (Figure 2A); gadolinium-enhanced MRI revealed a mild enhancement effect (Figure 2B); the T2-weighted image (T2WI) increased; and the fluid-attenuated inversion recovery (FLAIR) increased (Figure 2C). Of note, the diffusion-weighted imaging (DWI) showed mixed intensity (Figure 2D), while the apparent diffusion coefficient (ADC) was hyperintense (Figure 2E), which was primarily consistent with vasogenic edema. These features noted upon imaging motivated us to focus on the cerebral vein system. It is well known that the internal cerebral veins that receive venous blood from the medullary thalamic and thalamostriate veins converge with the basal veins of Rosenthal into the vein of Galen, and then with the inferior sagittal sinus from the straight sinus.4 After thrombosis of the vein of Galen and straight sinus develops, the venous drainage becomes blocked and vaDiagnosis: Thrombosis of the vein of Galen

Ganglioside as a neurotrophic drug has been hitherto widely used in China, although Guillain-Barré syndrome (GBS) following intravenous ganglioside treatment was reported in Europe several decades ago. We identified 7 patients who developed GBS after intravenous use of gangliosides (ganglioside+ group) and compared their clinical data with those of 77 non-ganglioside-associated GBS patients (ganglioside- group) in 2013, aiming at gaining the distinct features of ganglioside-associated GBS. Although the mean age, protein levels in cerebrospinal fluid (CSF) and frequency of cranial nerve involvement were similar between the two groups, the Hughes Functional Grading Scale (HFGS) score and the Medical Research Council (MRC) sum score at nadir significantly differed (4.9 ± 0.4 vs 3.6 ± 1.0; 7.7 ± 5.5 vs 36.9 ± 14.5, both p

Critical illness polyneuropathy and critical illness myopathy are frequent complications of severe illness that involve sensorimotor axons and skeletal muscles, respectively. Clinically, they manifest as limb and respiratory muscle weakness. Critical illness polyneuropathy/myopathy in isolation or combination increases intensive care unit morbidity via the inability or difficulty in weaning these patients off mechanical ventilation. Many patients continue to suffer from decreased exercise capacity and compromised quality of life for months to years after the acute event. Substantial progress has been made lately in the understanding of the pathophysiology of critical illness polyneuropathy and myopathy. Clinical and ancillary test results should be carefully interpreted to differentiate critical illness polyneuropathy/myopathy from similar weaknesses in this patient population. The present review is aimed at providing the latest knowledge concerning the pathophysiology of critical illness polyneuropathy/myopathy along with relevant clinical, diagnostic, differentiating, and treatment information for this debilitating neurological disease.

Dear Editors,Martins-De-Souza and colleagues reported elevated levels of apolipoprotein E (apoE) in the cerebrospinal fluid (CSF) from first-episode schizophrenia patients (Martins-De-Souza et al. ...

In the Letter to the Editor by Grant [1], the author suggested geographical differences in APOE genotype distribution as an alternative hypothesis to explain the inverse correlation between incident solar radiation and coronary heart disease (CHD) mortality rates in Western Europe. However, we have some concern about this hypothesis. Based on epidemiological investigations, geographical differences have been proposed in APOE aliele distribution in healthy population; the prevalence of the APOE4 aliele increases with latitude [2, 3]. As hypothesized by the author, fresh fruits and vegetables at higher latitudes are less readily available than at lower latitudes [4]; apoE4 protein can cause the liver to produce more cholesterol and the pancreas more insulin in order to store more food as fat; as a consequence, prevalence of the APOE4 aliele increases with latitude. In light of this statement, the APOE4 aliele seems to be an mutant of APOE 2 or 3 aliele, whereas this is not evidenced by evolutionary analysis, which implies APOE4 aliele as the ancestral aliele of APOE [5, 6]. Moreover, association does not necessarily mean causation, a vexing problem often raised and debated by epidemiologists [7]. In a recent review by Prakash et al. [8], the authors suggested a relation between prevalence of headache and the latitude. Similarly, although the profile of headache matches with seasonal variations and geographical distribution of serum vitamin D levels, we believe it far-fetched to propose such a correlation. According to our current knowledge, we can only ascribe this to coincidence

In a recent issue of Obesity Surgery, Iannelli and colleagues reported a case of a 27-year-old woman that developed diplopia, weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events 10 months after laparoscopic Roux-en-Y gastric bypass for morbid obesity. They established the diagnosis of Wernicke’s encephalopathy (WE) based on clinical manifestations as well as a 12-month follow-up [1]. This case is interesting because it provided general surgeons an insight into the overlooked diagnosis of WE after obesity surgery. However, we have some concerns about the differential diagnoses of this case. WE is defined as the combination of ataxia, ophthalmoplegia, nystagmus, and mental confusion resulting from vitamin B1 deficiency [2]. In their report, the authors did not detect the level of vitamin B1 in the serum. As a result, differential diagnoses should be distinguished from the diagnosis they proposed, i.e. WE. The patient was admitted at a peripheral hospital with severe dehydration and a history of persistent vomiting. We would like to know whether electrolyte disorders exist at that time. Electrolyte disorders such as hypopotassaemia and hyponatremia may present as quadriplegia, absent deep tendon reflexes, and disturbance of consciousness. We agree that thiamine plays a role in carbohydrate metabolism and the administration of glucose and other carbohydrates without thiamine can be dangerous for patients with thiamine deficiency, while extrapontine myelinolysis (EPM) due to rapid correction of severe hyponatremia should also be taken into account since the patient manifested diplopia, weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events after she was admitted by the authors [3]. Lesions in extrapontine myelinolysis have been increasingly documented, including cerebellum, lateral geniculate body, external and extreme capsules, hippocampus, putamen, cerebral cortex/subcortex, thalamus, and caudate nucleus. Unusual sites for EPM include spinal cord, mamillary bodies, amygdala, columns of the fornix, anterior commissure, optic tract, subthalamic nucleus, etc. The clinical manifestations, as a consequence, vary according to different lesions [4–8]. In WE, MRI may show a symmetrically increased T2 signal in the paraventricular regions of the thalamus, hypothalamus, mamillary bodies, and/or midline cerebellum [9]. However, MRI of this case showed only multiple ranges of subcortical edema in the occipital regions, which not only support the diagnosis of WE but also EPM. In addition, polyneuropathy is not uncommon in patients with vitamin B1 deficiency [10]. The patient was reported to have quadriplegia and absent deep tendon reflexes in knee and ankle joints bilaterally, whereas pathological signs, which are important in differentiating peripheral paralysis from central paralysis, were not reported. In particular, urinary incontinence that the patient presented with may be indicative of spinal cord involvement. K.-J. Zhang :D. Zhang Department of Plastic Surgery, The First Hospital of Jilin University, Changchun, China

WCN 2013 No: 56 Topic: 6 — MS & Demyelinating Diseases Postural orthostatic tachycardia syndrome associated with multiple sclerosis I. Adamec, M. Lovric, D. Zaper, A.K. Barusic, I. Bach, A. Mismas, M. Habek. UHC Zagreb, Zagreb, Croatia; University Hospital Center Zagreb, Zagreb, Croatia Background: Postural orthostatic tachycardia syndrome (POTS) is an autonomic disorder characterized by an exaggerated increase in heart rate that occurs during standing, without orthostatic hypotension. Objective: The aim of this study was to determine if there is a difference in the frequency of postural orthostatic tachycardia syndrome (POTS) in patients with multiple sclerosis (MS) compared to patients with symptoms of orthostatic intolerance and with no evidence of MS or other neurological illness. Methods: We analyzed data gathered from 293 (112 with MS and 181 without MS) patients who underwent the head-up tilt table test protocol. If POTS was identified the head-up tilt table test was repeated and supine and standing serum epinephrine and norepinephrine were determined. Results: POTS was identified in 39 patients: 21(19%) in the MS group compared to 18 (10%) in the non-MS group (p = 0.035). There was no difference between groups in the occurrence of POTS associated syncope (p = 0.52). There was no difference between groups in the epinephrine or norepinephrine in supine and standing positions. While both standing epinephrine and norepinephrine levels were significantly higher compared to laying levels in the non-MS group, only standing norepinephrine levels were significantly higher in the MS group. Conclusions: The results of this study suggest that POTS is associated with MS. doi:10.1016/j.jns.2013.07.1513 Abstract — WCN 2013 No: 66 Topic: 6 — MS & Demyelinating Diseases Pathogenetic role of T helper 17 cells and cytokines in Guillain–Barre syndrome WCN 2013 No: 66 Topic: 6 — MS & Demyelinating Diseases Pathogenetic role of T helper 17 cells and cytokines in Guillain–Barre syndrome H. Zhang, X. Wang, J. Zhu. Department of Neurology, First Hospital, Jilin University, Changchun, China; Karolinska Institute

Ylipalosaari and colleagues [1] reported an interesting case of Guillain–Barre syndrome (GBS) in a patient with ulceroglandular tularemia. Similar cases have been reported in the authors’ hospital [2] and another institution [3]. Clinically, GBS is characterized by the acute or subacute onset of varying degrees of weakness in limbs or cranial nerve-innervated muscles, associated with characteristic albuminocytologic dissociation in the cerebrospinal fluid (CSF). GBS is usually preceded by various infections. About two-thirds of cases are preceded by symptoms of upper respiratory tract infection or diarrhea [4]. In this case, however, the clinical course of weakness of limbs and respiratory muscles paralleled that of ulceroglandular tularemia too perfectly. This is concomitant with the ineffectiveness of intravenous immunoglobulin. Moreover, the characteristic albuminocytologic dissociation in the CSF was absent for this patient. As mentioned by the authors, there have been reports of tularemia meningitis and intracranial abscesses [5]. The elevated number of white blood cells in the CSF (we believe that the real number should be 47 9 10/L, instead of 47/L in the text) strongly suggests direct involvement of the nervous system by pathogens. Taken together, the atypical clinical manifestations of the patient prompt us to consider other differential diagnoses, including infectious polyneuritis, critical illness polyneuropathy (CIP) and myopathy (CIM), etc.

Background Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are complications causing weakness of respiratory and limb muscles in critically ill patients. As an important differential diagnosis of Guillain-Barré syndrome (GBS), CIP and CIM should be diagnosed with caution, after a complete clinical and laboratory examination. Although not uncommon in ICU, CIP and CIM as severe complications of percutaneous nephrostolithotomy (PNL) have not been documented in literature. Case presentation A 48-year-old Chinese woman was referred to our hospital, complaining of occasional pain in the right lower back for one month. Lithiasis was diagnosed by ultrasonographical and radiological examinations on the urinary system. PNL was indicated and performed. The patient developed CIP and CIM on the fourth day after PNL. Early recognition and treatment of the severe complications contributed to a satisfactory recovery of the patient. Conclusion This case expands our understanding of the complications of PNL and underscores the importance of differentiating CIP/CIM from GBS in case of such patients developing weakness after the treatment. Clinical characteristics and examination results should be carefully evaluated to make the diagnosis of CIP or CIM. Both anti-septic prophylaxis and control of hyperglycemia might be effective for the prevention of CIP or CIM; aggressive treatment on sepsis and multiple organ failure is considered to be the most effective measure to reduce the incidence of CIP/CIM.

The role that the carboxyl-terminal amino acids of Escherichia coli DNA topoisomerase I (Topo I) and III (Topo III) play in catalysis was examined by comparing the properties of Topo III with those of a truncated enzyme lacking the generalized DNA binding domain of Topo III, Topo I, and a hybrid topoisomerase polypeptide containing the amino-terminal 605 amino acids of Topo III and the putative generalized DNA binding domain of Topo I. The deletion of the carboxyl-terminal 49 amino acids of Topo III decreases the affinity of the enzyme for its substrate, single-stranded DNA, by approximately 2 orders of magnitude and reduces Topo III-catalyzed relaxation of supercoiled DNA and Topo III-catalyzed resolution of DNA replication intermediates to a similar extent. Fusion of the carboxyl-terminal 312 amino acid residues of Topo I onto the truncated molecule stimulates topoisomerase-catalyzed relaxation 15-20-fold, to a level comparable with that of full-length Topo III. However, topoisomerase-catalyzed resolution of DNA replication intermediates was only stimulated 2-3-fold. Therefore, the carboxyl-terminal amino acids of these topoisomerases constitute a distinct and separable domain, and this domain is intimately involved in determining the catalytic properties of these polypeptides.

The role of tumor necrosis factor (TNF)-α and its receptors in neuroautoimmune and neuroinflammatory diseases has been controversial. On the basis of our previous studies, we hereby aimed to further clarify TNF-α’s mechanism of action and to explore the potential role of TNF-α receptor (TNFR)1 as a therapeutic target in experimental autoimmune neuritis (EAN). EAN was induced by immunization with P0 peptide 180–199 in TNF-α knockout (KO) mice and anti-TNFR1 antibodies were used to treat EAN. Particularly, the effects of TNF-α deficiency and TNFR1 blockade on macrophage functions were investigated. The onset of EAN in TNF-α KO mice was markedly later than that in wild type (WT) mice. From day 14 post immunization, the clinical signs of TNF-α KO mice were significantly milder than those of their WT counterparts. Further, we showed that the clinical severity of WT mice treated with anti-TNFR1 antibodies was less severe than that of the control WT mice receiving PBS. Nevertheless, no difference with regard to the clinical signs of EAN or inflammatory infiltration in cauda equina was seen between TNF-α KO and WT mice with EAN after blockade of TNFR1. Although TNF-α deficiency did not alter the proliferation of lymphocytes in response to either antigenic or mitogenic stimuli, it down-regulated the production of interleukin (IL)-12 and nitric oxide (NO), and enhanced the production of IL-10 in macrophages. Increased ratio of regulatory T cells (Tregs) and reduced production of interferon (IFN)-γ in cauda equina infiltrating cells, and elevated levels of IgG2b antibodies against P0 peptide 180–199 in sera were found in TNF-α KO mice with EAN. In conclusion, TNF-α deficiency attenuates EAN via altering the M1/M2 balance of macrophages.

Atomic scale investigation of temperature-dependent two-dimensional (2 D) crystallization processes of fullerene-C60 on pentacene-covered Ag(111) surface has been carried out by in situ low-temperature scanning tunneling microscopy (LT-STM) experiments. To evaluate the effect of molecule-substrate interfacial interactions on the 2 D crystallization of C60: pentacene binary system, we also carried out the same self-assembly experiments of C60 on monolayer pentacene covered graphite substrate. It is revealed that temperature-dependent structural transition of various ordered C60 nanoassemblies is strongly influenced by the molecule-Ag(111) interfacial interactions, and further mediated by the weak C60-pentacene intermolecular interactions. In situ ultraviolet photoelectron spectroscopy (UPS) has been used to evaluate the nature of the intermolecular interactions between C60 and pentacene films.

C6-azolyl purine nucleoside products are prepared in high yields under solvent- and catalyst-free conditions via C–N coupling reaction of unprotected 6-chloropurine nucleosides and N-heterocycles, providing a unifying, simple and environmentally friendly complement to the available methods.