Genome-wide Analysis of Glucose-6-phosphate Dehydrogenase(G6PDH) and Its Evolution in Eucalyptus grandsis

[Objective] The aim of this study was to perform genome-wide analysis of glucose-6-phosphate dehydrogenase（G6PDH） and reveal its evolution in Eucalyptus grandsis.[Method] The gene character,protein sequence and phylogenetic tree of G6PDH gene were analyzed by BLAST and other bioinformatics software within Eucalyptus grandsis whole genome database.[Result] Six G6PDH genes,including one cytomic type and five plastids,were detected in the E.grandsis genome.All the G6PDHs have conserved motifs of motif 1,motif 2,motif 3,motif 7,motif 9 and motif 11.Furthermore,promoter sequences of all E.grandsis G6PDH contain TATA box,enhancer,light-responsive,hormone-responsive and stress-responsive regulatory elements.[Conclusion] This study provided reference for the further revealing molecular function of E.grandsis G6PDH gene family

Cloning and Sequence Analysis of a Glucose-6-Phosphate Dehydrogenase Gene PsG6PDH from Freezing-tolerant Populus suaveolens

A 1 207 bp cDNA fragment (PsG6PDH) was amplified by RT-PCR from cold-induced total RNA of the freez- ing-tolerant P. Suaveolens, using primers based on the highly conserved region of published plant glucose-6-phosphate dehydro- genase (G6PDH) genes. The sequence analysis showed that PsG6PDH coding region had 1 101 bp and encoded 367 predicted amino acid residues. Moreover, the nucleotide sequence of PsG6PDH showed 83%, 82%, 79%, 79% and 78% identity, and the derived amino acid sequence shared 44.2%, 44.7%, 42.0%, 40.5% and 43.9% identity with those of the Solanum tuberosum, Nicotiana ta- bacum, Triticum aestivum, Oryza sativa and Arabidopsis thaliana, respectively. The results show that PsG6PDH is a new member of G6PDH gene family and belongs to the cytosolic G6PDH gene. This is the first report on cloning of the G6PDH gene from woody plants.

Involvement of the circular RNA/microRNA/glucose-6-phosphate dehydrogenase axis in the pathological mechanism of hepatocellular carcinoma

Hepatocellular carcinoma(HCC)is the third most common cause of cancer-related death worldwide with high mortality.The incidence of HCC is increasing in China.Abnormal activation of glucose-6-phosphate dehydrogenase(G6 PD)exists in all malignant tumors,including HCC,and is closely related to the development of HCC.In addition,the differential expression of non-coding RNAs is closely related to the development of HCC.This systematic review focuses on the relationship between G6 PD,HCC,and noncoding RNA,which form the basis for the circ RNA/mi RNA/G6 PD axis in HCC.The circular RNA(circ RNA)/micro RNA(mi RNA)/G6 PD axis is involved in development of HCC.We proposed that non-coding RNA molecules of the circ RNA/mi RNA/G6 PD axis may be novel biomarkers for the pathological diagnosis,prognosis,and targeted therapy of HCC.

Is glucose-6-phosphate dehydrogenase deficiency more prevalent in Carrion's disease endemic areas in Latin America?

Glucose-6-phosphate dehydrogenase(G6PD) is a cytoplasmic enzyme with an important function in cell oxidative damage prevention.Erythrocytes have a predisposition towards oxidized environments due to their lack of mitochondria,giving G6 PD a major role in its stability.G6 PD deficiency(G6PDd) is the most common enzyme deficiency in humans:it affects approximately 400 million individuals worldwide.The overall G6 PDd allele frequency across malaria endemic countries is estimated to be 8%.corresponding to approximately 220 million males and 133 million females.However,there are no reports on the prevalence of G6 PDd in Andean communities where bartonellosis is prevalent.

Prevalence of Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency in India: A Systematic Review

Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is the most common enzyme deficiency of human erythrocyte affecting more than 400 million people worldwide. In India, G6PD deficiency was first reported in 1963 and since then various investigations have been conducted across country. The objective of this work was to study the prevalence of G6PD deficiency in different ethnic, caste and linguistic groups of Indian population. A systematic search of published literature was undertaken and the wide variability of G6PD deficiency has been observed ranging from 0% - 30.7% among the different caste, ethnic, and linguistic groups of India. It was observed that the incidence of G6PD deficiency was found to be considerably higher among the tribes (9.86%) as compared to other ethnic groups (7.34%) and significantly higher in males as compared to females.

Purification and Characterization of Glucose-6-Phosphate Dehydrogenase from Pigeon Pea (Cajanus cajan) Seeds

Glucose-6-phosphate dehydrogenase has been purified from pigeon pea (Cajanus cajan) seeds and subjected to characterization. The enzyme was purified 123.69 fold with a yield of 21.37% by ammonium sulphate fractionation, PEG-4000 precipitation, CM cellulose column chromatography and DEAE cellulose column chromatography. The catalytically active enzyme is a dimer of 113 KDa with a subunit molecular weight of 55 KDa. Thermal inactivation of enzyme follows first order kinetics at 30&#176C and 40&#176C with half life of 6 and 1.5 min respectively. Km value for glucose-6-phosphate and NADP+ was found to be 2.68 mM and 0.75 mM respectively whereas Vmax value was found to be 0.11 U/mL and 0.13 U/mL respectively. The enzyme shows more affinity towards NADP+ than glucose-6-phosphate. The pKa value was found to be 10.41 indicating that the amino acid residue at active site might be lysine. The enzyme exhibited maximum catalytic activity at pH 8.2. The enzyme was found to be highly thermosensitive with gradual loss of activity above 30&#176C temperature.

Glucose-6-phosphate dehydrogenase(G6PD) deficiency is associated with asymptomatic malaria in a rural community in Burkina Faso

Objective:To investigate 4 combinations of mutations responsible for glucose-6—phosphate dehydrogenase(G6PD) deficiency in a rural community of Burkina Faso,a malaria endemic country.Methods:Two hundred individuals in a rural community were genotyped for the mutations A376 G.G202A,A542 T,G680T and T968 C using TaqMan single nucleotide polymorphism assays and polymerase chain reaction followed by restriction fragment length polymorphism.Results:The prevalence of the G6 PD deficiency was 9.5%,in the study population.It was significantly higher in men compared to women(14.23%vs 6.0%,P=0.049).The 202A/376 G G6PD Awas the only deficient variant detected.Plasmodium falciparum asymptomatic parasitemia was significantly higher among the C6PD-non—deficient persons compared to the G6PD-deficient(P<0.001).The asymptomatic parasitemia was also significantly higher among G(SPI) nondeficient compared to C6PD—heterozygous females(P<0.001).Conclusions:This study showed that the G6 PD A- variant associated with protection against asymptomatic malaria in Burkina Faso is probably the most common deficient variant.

Is there any role of glucose-6-phosphate dehydrogenase in obesity induced metabolic disorder

The present study was designed to explore the possible mechanism of obesity associated metabolic syndrome. 150 subjects (120 men and 30 women) in the age-group of 17 - 26 years were studied. Body Mass Index and Waist-to-Hip Ratio were taken as a measure of generalized obesity and abdominal adiposity. The serum concentration of glucose-6-phosphate dehydrogenase increased with increasing levels of Body Mass Index and was found to be significant in obese subjects (Body Mass Index ≥ 30.0 kg/m2) and more so in the obese subjects with abdominal adiposity (p = 0.002) as compared to normal-weight subjects. Karl Pearson coefficient of correlation revealed a significant positive correlation of glucose-6-phosphate dehydrogenase with Body Mass Index (r = 0.499;p < 0.001) and malondialdehyde (a biomarker of oxidative stress) (r = 0.736;p < 0.001) but inverse correlation with adiponectin (r = -0.524;p < 0.001). Thus, we conclude that increased expression of glucose-6-phosphate dehydrogenase in obese subjects (more if it is associated with abdominal adiposity) might mediate the onset of obesity associated metabolic disorders by increasing oxidative stress.

HEXOKINASE, GLUCOSE-6-PHOSPHATASE DEHYDROGENASE AND ALEOSE REDUCTASE IN HUMAN FETAL LENSES

The lens HK, G6PD, AR activity and its relationship with fetal age was determined.There is a positive correlation between the age of fetus and the activity(IU/mg pro.) of HK and G6PD(r=0.8069, 0.8204, P<0.01) and a negetive correlation between the age of fetus and activity of AR(r=-0.810 1,0.05>P>0.01).

Characterization of glucose-6-phosphate dehydrogenase deficiency and identification of a novel haplotype 487G>A/IVS5-612(G>C) in the Achang population of southwestern China

The prevalence of glucose-6-phosphate dehydrogenase (G6PD) deficiency and its gene mutations were studied in the Achang population from Lianghe County in Southwestern China. We found that 7.31% (19 of 260) males and 4.35% (10 of 230) females had G6PD deficiency. The molecular analysis of G6PD gene exons 2―13 was performed by a PCR-DHPLC-Sequencing or PCR-Sequencing. Sixteen inde-pendent subjects with G6PD Mahidol (487G>A) and the new polymorphism IVS5-612 (G>C), which combined into a novel haplotype, were identified accounting for 84.2% (16/19). And 100% Achang G6PD Mahidol were linked to the IVS5-612 C. The percentage of G6PD Mahidol in the Achang group is close to that in the Myanmar population (91.3% 73/80), which implies that there are some gene flows between Achang and Myanmar populations. Interestingly, G6PD Canton (1376G>T) and G6PD Kaiping (1388G>A), which were the most common G6PD variants from other ethnic groups in China, were not found in this Achang group, suggesting that there are different G6PD mutation profiles in the Achang group and other ethnic groups in China. Our findings appear to be the first documented report on the G6PD genetics of the AChang people, which will provide important clues to the Achang ethnic group origin and will help prevention and treatment of malaria in this area.

G6PT-H6PDH-11βHSD1 triad in the liver and its implication in the pathomechanism of the metabolic syndrome

The metabolic syndrome, one of the most common clinical conditions in recent times, represents a combination of cardiometabolic risk determinants, including central obesity, glucose intolerance, insulin resistance, dyslipidemia, non-alcoholic fatty liver disease and hypertension. Prevalence of the metabolic syndrome is rapidly increasing worldwide as a consequence of common overnutrition and consequent obesity. Although a unifying picture of the pathomechanism is still missing, the key role of the pre-receptor glucocorticoid activation has emerged recently. Local glucocorticoid activation is catalyzed by a triad composed of glucose-6-phosphate-transporter, hexose-6-phosphate dehydrogenase and 11β-hydroxysteroid dehydrogenase type 1 in the endoplasmic reticulum. The elements of this system can be found in various cell types, including adipocytes and hepatocytes. While the contribution of glucocorticoid activation in adipose tissue to the pathomechanism of the metabolic syndrome has been well established, the relative importance of the hepatic process is less understood. This review summarizes the available data on the role of the hepatic triad and its role in the metabolic syndrome, by confronting experimental findings with clinical observations.

Molecular Cloning of a Cytosolic G6PDH Gene from Populus Suaveolens and Its Expression to Improve the Cold Resistance of Tobacco Plants

Glucose-6-phosphate dehydrogenase (G6PDH,EC 1.1.1.49) is the first and main regulated enzyme of oxidative pentose phosphate pathway (OPPP),catalyzing the conversion of glucose-6-phosphate to 6-phospho-gluconolactone and playing important roles in the growth and development of plants. It is preciously reported that the enhancement of freezing resistance of Populus suaveolenscuttings is clear related to the distinct increase in cytosolic G6PDH activity. Here,a 1697 bp cDNA fragment (PsG6PDH) is amplified by RT-PCR from cold-induced total RNA of the freezing-tolerant P. suaveolens. A sequence analysis showed that PsG6PDH coding region had 1 530 bp and encoded 510 predicted amino acid residues. Genomic Southern analysis revealed that the isoform is encoded by a few copies of the gene in the poplar genome. The cloned gene PsG6PDHis cloned into binary vector pBI121 and used to transform tobacco. PCR and Southern blotting results verified integration of this gene into the genome of tobacco. Moreover,cold treatment experiments and membrane defense enzymeactivity analysis confirmed that overexpression of the PsG6PDHgene could enhance the tolerance to cold or frigid stresses in transgenic plants.

The fungal endophyte Epichloëgansuensis increases NaCltolerance in Achnatherum inebrians through enhancing the activity of plasma membrane H^(+)-ATPase and glucose-6-phosphate dehydrogenase

Salt stress negatively affects plant growth,and the fungal endophyte Epichloëgansuensis increases the tolerance of its host grass species,Achnatherum inebrians,to abiotic stresses.In this work,we first evaluated the effects of E.gansuensis on glucose-6-phosphate dehydrogenase(G6PDH)and plasma membrane(PM)H^(+)-ATPase activity of Achnatherum inebrians plants under varying NaCl concentrations.Our results showed that the presence of E.gansuensis increased G6PDH,PMH^(+)-ATPase,superoxide dismutase and catalase activity to decrease O2•^(–),H_(2)O_(2)and Na^(+)contents in A.inebrians under NaCl stress,resulting in enhanced salt tolerance.In addition,the PM NADPH oxidase activity and NADPH/NADP+ratios were all lower in A.inebrians with E.ganusensis plants than A.inebrians plants without this endophyte under NaCl stress.In conclusion,E.gansuensis has a positive role in improving host grass yield under NaCl stress by enhancing the activity of G6PDH and PM H^(+)-ATPase to decrease ROS content.This provides a new way for the selection of stress-resistant and high-quality forage varieties by the use of systemic fungal endophytes.

Etiology analysis for term newborns with severe hyperbilirubinemia in eastern Guangdong of China

BACKGROUND Neonatal hyperbilirubinemia is one of the common diseases of newborns that typically presents with yellow staining of skin,resulting in sequelaes such as hearing loss,motor and intellectual development disorders,and even death.The pathogenic factors of neonatal hyperbilirubinemia are complex.Different cases of hyperbilirubinemia may have a single or mixed etiology.AIM To explore the etiological characteristics of severe hyperbilirubinemia in term newborns of eastern Guangdong of China.METHODS Term newborns with severe hyperbilirubinemia in one hospital from January 2012 to December 2021 were retrospectively analyzed.The etiology was determined according to the laboratory results and clinical manifestations.RESULTS Among 1602 term newborns with hyperbilirubinemia in eastern Guangdong of China,32.20%(580/1602)was severe hyperbilirubinemia.Among the causes of severe hyperbilirubinemia,neonatal hemolysis accounted for 15.17%,breast milk jaundice accounted for 12.09%,infection accounted for 10.17%,glucose-6-phosphate dehydrogenase(G6PD)deficiency accounted for 9.14%,and the coexistence of multiple etiologies accounted for 6.55%,unknown etiology accounted for 41.72%.ABO hemolysis and G6PD deficiency were the most common causes in the 20 cases with bilirubin encephalopathy.94 severe hyperbilirubinemia newborns were tested for uridine diphosphate glucuronosyl transferase 1A1(UGT1A1)*6 variant(rs4148323,c.211G>A,p.Arg71Gly),9 cases were 211 G to A homozygous variant,37 cases were 211 G to A heterozygous variant,and 48 cases were wild genotypes.CONCLUSION The main cause for severe hyperbilirubinemia and bilirubin encephalopathy in eastern Guangdong of China were the hemolytic disease of the newborns,G6PD deficiency and infection.UGT1A1 gene variant was also a high-risk factor for neonatal hyperbilirubinemia.Targeted prevention and treatment according to the etiology may reduce the occurrence of bilirubin encephalopathy and kernicterus.

The 6-phosphogluconate Dehydrogenase Genes Are Responsive to Abiotic Stresses in Rice

Glucose-6-phosphate dehydrogenase （G6PDH, E.C. 1.1.1.49） and 6-phosphogluconate dehydrogenase （6PGDH, EC 1.1.1.44） are both key enzymes of the pentose phosphate pathway （PPP）. The OsG6PDH1 and Os6PGDH1 genes encoding cytosolic G6PDH and cytosolic 6PGDH were Isolated from rice （Oryza sativa L.）. We have shown that Os6PGDH1 gene was up-regulated by salt stress. Here we reported the isolation and characterization of Os6PGDH2 from rice, which encode the plastidic counterpart of 6PGDH. Genomic organization analysis indicated that OsG6PDH1 and OsG6PDH2 genes contain multiple introns, whereas two Os6PGDH1 and Os6PGDH2 genes have no introns in their translated regions. In a step towards understanding the functions of the pentose phosphate pathway in plants in response to various abiotic stresses, the expressions of four genes in the rice seedlings treated by drought, cold, high salinity and abscisic acid （ABA） were investigated. The results show that OsG6PDH1 and OsG6PDH2 are not markedly regulated by the abiotic stresses detected. However, the transcript levels of both Os6PGDH1 and Os6PGDH2 are up-regulated in rice seedlings under drought, cold, high salinity and ABA treatments. Meanwhile, the enzyme activities of G6PDH and 6PGDH in the rice seedlings treated by various abiotic stresses were Investigated. Like the mRNA expression patterns, G6PDH activity remains constant but the 6PGDH Increases steadily during the treatments. Taken together, we suggest that the pentose phosphate pathway may play an important role in rice responses to abiotic stresses and the second key enzyme of PPP, 6PGDH, may function as a regulator controlling the efficiency of the pathway under abiotic stresses.

Selection of oocytes for in vitro maturation by brilliant cresyl blue staining： a study using the mouse model

Selecting oocytes that are most likely to develop is crucial for in vitro fertilization and animal cloning. Brilliant cresyl blue （BCB） staining has been used for oocyte selection in large animals, but its wider utility needs further evaluation. Mouse oocytes were divided into those stained （BCB＋） and those unstained （BCB-） according to their ooplasm BCB coloration. Chromatin configurations, cumulus cell apoptosis, cytoplasmic maturity and developmental competence were compared between the BCB＋ and BCB- oocytes. The effects of oocyte diameter, sexual maturity and gonadotropin stimulation on the competence of BCB＋ oocytes were also analyzed. In the large- and medium-size groups, BCB＋ oocytes were larger and showed more surrounded nucleoli （SN） chromatin configurations and higher frequencies of early atresia, and they also gained better cytoplasmic maturity （determined as the intracellular GSH level and pattern of mitochondrial distribution） and higher developmental potential after in vitro maturation （IVM） than the BCB-oocytes. Adult mice produced more BCB＋ oocytes with higher competence than the prepubertal mice when not primed with PMSG. PMSG priming increased both proportion and developmental potency of BCB＋ oocytes. The BCB＋ oocytes in the large-size group showed more SN chromatin configurations, better cytoplasmic maturity and higher developmental potential than their counterparts in the medium-size group. It is concluded that BCB staining can be used as an efficient method for oocyte selection, but that the competence of the BCB＋ oocytes may vary with oocyte diameter, animal sexual maturity and gonadotropin stimulation. Taken together, the series of criteria described here would allow for better choices in selecting oocytes for better development.

Comparisons of different methods of anesthesia and analgesia on the levels of glycometabolism rate-limiting enzymes in erythrocytes and plasma glucose and stress hormones in patients undergoing esophagus surgery

Objective： To compare the effects of different methods of anesthesia and analgesia on the activities of phosphofructokinase（PFK）, glucose-6-phosphate dehydrogenase（G-6PD） and aldose reductase（AR） in erythrocytes and levels of plasma glucose and stress hormones in patients undergoing esophagus surgery. Methods： Sixty-two patients scheduled for esophagus surgery were randomly divided into three groups： group Ⅰ （n = 20） receiving only general anesthesia（GA） followed by intravenous patient controlled analgesia（PCA） with fentanyl 15 μg/kg. The other two groups receiving both general anesthesia combined with thoracic epidural anesthesia （GEA） and either intravenous PCA with fentanyl 15 μg/kg （group Ⅱ, n = 21） or thoracic epidural analgesia（TEA） with 0.125% ropivacaine and 0.0002% fentanyl mixture（group Ⅲ, n = 21） after the operation. Venous blood samples were collected for measurements of PFK, G-rPD and AR activities in erythrocytes and plasma glucose, cortisol, epinephrine and norepinephrine before induction （T1）, 60 min following the incision （T2）, 60 min（T3） after operation, on the lst（T4） and 2nd postoperative day（T5）. Results： The activities of PFK decreased（P 〈 0.01 or P = 0.004） and the activities of G-6PD and AR increased（P 〈 0.01） in groups Ⅰ and Ⅱ on T4 compared with those on T1 Between the two groups, the activities of these enzymes in group Ⅱ changed less than those of group Ⅰ （P 〈 0.01 or P 〈 0.05）. These enzymes activities changed slightly in group Ⅲ on T4（P 〉 0.05）. There were significant differences between group Ⅲand the other two groups（P 〈 0.0l or P 〈 0.05）. The levels of plasma glucose increased significantly on T2（P 〈 0.01）, reached peak values on Ta（P 〈 0.01） and fell on T5 in the three groups. Compared to those of groups Ⅰ and Ⅱ, the values of plasma glucose in group Ⅲwere lower on T4 and T5（P 〈 0.05 or P 〈 0.01）. The cortisol concentration in each group increased significantly at T2（P 〈 0.01 or P 〈 0.05）, and remained elevated on T5（P 〈 0.01 or P 〈 0.05）, while on T2 and T3 the cortisol levels＇ of group I were higher than that of groups Ⅱand Ⅲ （P 〈 0.05）. The levels of group Ⅲ were lower than those of the other groups on T4 and T5（P 〈 0.01 or P 〈 0.05）. The levels of epinephrine and norepinephrine were also significantly higher in group Ⅰ than those of the other two groups on T2（P 〈 0.01 or P 〈 0.05）, and their levels in group Ⅰ and Ⅱ were higher than that of group Ⅲ on T4. The patients of the three groups obtained satisfactory pain relief, with all Vidual Analogue Scale（VAS） scores less than 3. VAS scores of group I were much greater 4h after operation. Group m VAS scores were the lowest 24h after operation. However, the number of times patients pressed the bolus switch was higher in group Ⅱ （P 〈 0.01）. Conclusion： Compared with GA and intravenous PCA, general anesthesia combined with thoracic epidural anesthesia and analgesia obtain better pain relief and could markedly alleviate the stress response and improve these erythrocyte glucose metabolism changes after esophagus surgery.

The high incidence of acute hemolysis due to favism in Ahvaz,Iranclinical features and laboratory findings

Objective:To collect comprehensive information about the features of favic patients in Ahvaz (Capital of Khouzestan,Iran) and analyze the extent of the differences with their corresponding in other regions.Methods:A total of 103 patients with acute hemolysis admitted to pediatric division of Abouzar Hospital located in the city of Ahvaz,Iran during 21st of June 2008 to 20th of June 2009 were analyzed retrospectively.Results:95.14% of the patients had favism while 4.86% of them underwent hemolysis due to other reasons.These patients were male(68.93%) and female children(31.06%) admitted mostly during the spring season.The three main symptoms were urine discoloration,jaundice and vomiting.At the admission time,the main hematologic findings were as follows:G6PD sufficient status(45.63%),G6PD deficient status(54.36%) and hemoglobin concentration:2.5-11.8(mean±SD:6.45±2.12) g/dL.Conclusions:In conclusion,Ahvaz was determined as a black zone for favism in which the disease can be considered a life threatening health problem.Moreover,slight differences were observed in the three main symptoms compared with favic patients in other regions.

Hepatic retinaldehyde deficiency is involved in diabetes deterioration by enhancing PCK1-and G6PC-mediated gluconeogenesis

Type 2 diabetes(T2D) is often accompanied with an induction of retinaldehyde dehydrogenase 1(RALDH1 or ALDH1A1) expression and a consequent decrease in hepatic retinaldehyde(Rald)levels. However, the role of hepatic Rald deficiency in T2D progression remains unclear. In this study, we demonstrated that reversing T2D-mediated hepatic Rald deficiency by Rald or citral treatments, or liverspecific Raldh1 silencing substantially lowered fasting glycemia levels, inhibited hepatic glucogenesis,and downregulated phosphoenolpyruvate carboxykinase 1(PCK1) and glucose-6-phosphatase(G6PC)expression in diabetic db/db mice. Fasting glycemia and Pck1/G6pc mRNA expression levels were strongly negatively correlated with hepatic Rald levels, indicating the involvement of hepatic Rald depletion in T2D deterioration. A similar result that liver-specific Raldh1 silencing improved glucose metabolism was also observed in high-fat diet-fed mice. In primary human hepatocytes and oleic acidtreated HepG2 cells, Rald or Rald + RALDH1 silencing resulted in decreased glucose production and downregulated PCK1/G6PC mRNA and protein expression. Mechanistically, Rald downregulated direct repeat 1-mediated PCK1 and G6PC expression by antagonizing retinoid X receptor a, as confirmed by luciferase reporter assays and molecular docking. These results highlight the link between hepatic Rald deficiency, glucose dyshomeostasis, and the progression of T2D, whilst also suggesting RALDH1 as a potential therapeutic target for T2D.

Neonatal pyknocytosis in a preterm dizygotic twin

Infantile pyknocytosis(IP) is a rare, self-limited neonatal haemolytic anaemia that may require multiple blood transfusions. Only a little more than 50 cases have been reported in the medical literature, and the great majority of them concerns term infants. The etiology of IP is not well understood; most likely it results from a transient extra-corpuscular factor, whose nature is unknown, transmitted from mother to child or, alternatively, from a deficiency of an anti-oxidative agent. We report the case of two preterm twins, one of which suffered from IP and developed severe anaemia at age 2 wk, while the other was unaffected. Although no specific agent was identified as the cause of anaemia and IP, we speculate that the transmission of an agent from mother to child was unlikely, as only twin one suffered from IP. Smelly greenish diarrhoea occurred just before the presentation of IP, suggesting that the same agent led to both the diarrhoea and the oxidative injury. Because IP may remain underdiagnosed, it should be considered in cases of early unexplained severe hemolytic anemia.