Incorporating genotyping to identify patients with G6PD deficiency

Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a common X-linked enzyme disorder associated with hemolytic anemia after exposure to certain medications or foods. Activity testing is the gold standard for detecting G6PD deficiency; however, this test is affected by various hematologic parameters. Clinical G6PD genotyping is included in pharmacogenetic arrays and clinical sequencing and may be reconciled with activity results. Methods: Patients (n=1,391) enrolled on an institutional pharmacogenetic testing protocol underwent clinical G6PD genotyping for 164 G6PD variants. For the 446 patients with G6PD activity results, algorithms were designed to assign G6PD status, accounting for known interferences with the activity assay and for G6PD genotype results. We developed clinical decision support alerts to inform prescribers when high-risk medications were prescribed, warning of gene-drug interactions and recommending therapy alteration. Results: Of 1,391 patients with genotype, 1,334 (95.9%) patients were predicted to have normal G6PD activity, 30 (2.1%) were predicted to have variable G6PD activity, and 27 (2%) were predicted to have deficient G6PD activity. Of the 417 patients with a normal genotype and an activity result, 415 (99.5%) had a concordant normal G6PD phenotype. Of the 21 patients with a deficient genotype and an activity result, 18 (85.7%) had a concordant deficient activity result. Genotyping reassigned phenotype in 5 patients with discordant genotype and activity results: 3 switched from normal to deficient, and 2 switched from deficient to normal. Conclusion: G6PD activity and genotyping are two independent testing methods which can be used in conjunction to assign a more informed G6PD phenotype.

Serum Levels of Glutamate-Pyruvate Transaminase, Glutamate-Oxaloacetate Transaminase and Gamma-Glutamyl Transferase in 1494 Patients with Various Genotypes for the Alpha-1 Antitrypsin Gene

Background: Patients with liver disease associated with alpha-1 antitrypsin deficiency (AATD) are homozygous for the Z mutation, leading to chronic liver damage. Objective: To assess the serum levels of glutamate-oxaloacetate transaminase (GOT), glutamate-pyruvate transaminase (GPT), and gamma-glutamyl transpeptidase (GGT) in patients with different genotypes for the alpha-1 antitrypsin (AAT) gene. Methods: Patients (n = 1494) underwent genotyping of the SERPINA1 gene, together with a determination of AAT and GOT and GPT and GGT transaminase levels. Patients with a deficient allele (n = 476) and with a normal genotype were compared. Results: A statistically significant association was found between deficient genotypes and GOT (p < 0.0003), GPT (p < 0.002), and GGT (p < 0.006). Comparing GOT levels in patients with PI*Z deficient variant versus those with normal genotype, an odds ratio (OR) of 2.72 (CI: 1.5–4.87) (p < 0.0005) was obtained. This finding was replicated with the PI*Z allele and the GPT values (OR = 2.31; CI: 1.45–3.67; p < 0.0003). In addition, a statistically significant association was found between liver enzymes and AAT values. Conclusion: The PI*Z allele seemed to be a risk factor for the development of liver damage. AAT deficient genotypes were associated with GOT, GPT, and GGT altered values. Low AAT levels were associated with high GPT and GGT levels.

Influence of urokinase gene-knockout in C57BL/6-PlautmI. IBugThisPlau6FDhu/GFDhu mice on growth factors in malignant melanoma

Purpose of the study. Studying characteristics of the growth factor dynamics in the intact skin, tumors and perifocal tissues of melanoma in urokinase (uPA) gene-knockout mice.Materials and methods. The study included male and female С57 ВL/6 mice (n=47) and C57BL/6‑Plautm1.1BugThisPlauGFDhu/GFDhu mice with uPA gene-knockout (n=31). В16/F10 melanoma was transplanted subcutaneously at a dose of 0.5 mL (1:10 in normal saline). Intact mice of the same strain served as controls. Levels of VEGFA, VEGFC, sVEGFR1, sVEGFR3, IGF1, IGF2, TGFβ1 and FGF21 were determined by ELISA in the skin, tumor and perifocal tissues isolated on the 21st day of the tumor growth.Results. uPA gene-knockout inhibited the growth (mostly in females) and metastasis (predominantly in males) of melanoma in mice. Inhibition of the migration of malignant cells in males could be due to low levels of TGF-β1 compared to С57 ВL/6 mice: in the skin – by 5.0 times, in tumors – by 1.8 times and in perifocal tissues – by 6.1 times. In uPA gene-knockout females, lower levels of TGF-β1 were observed in tumors – by 1.4 times inhibited metastasis, but not completely, and solitary metastatic foci were registered in the lungs. Нigh levels of IGF1 in tissues of all uPA gene-knockout mice (males: in tumors by 1.4 times, in perifocal tissues by 2.6 times, in the skin by 3.6 times; females: in tumors by 2.6 times, in perifocal tissues by 25.0 times, in the skin by 13.9 times, compared to С57 ВL/6 mice) could maintain the metastatic phenotype of cancer cells (in females) or hiher proliferative activity of melanoma cells (in males). Lower levels of FGF‑21 in tumors (males – by 5.3 times, females – by 18.4 times), perifocal tissues (males – by 9.6 times, females – by 8,5 times) and skin (males – by 6.7 times, females – by 3.3 times) in uPA gene-knockout animals could be due to the IGF‑1 growth, as their reciprocal interaction is known. Interestingly, a significant, although lesser than in mice with a normal genotype, accumulation of VEGFA in melanoma tissues was observed: in males – in tumors by 44.9 times, in perifocal tissues by 6.8 times, in the skin by 2.4 times; in females – in tumors by 5.6 times, in perifocal tissues by 2.6 times, in the skin by 3.3 times, compared to the corresponding intact controls, due to the probable involvement of the uPA receptor (uPAR) in the implementation of VEGF-induced processes.Conclusion. Changing the activity of a system of some growth factors, uPA gene-knockout modifies melanoma metabolism by inhibiting its growth and eliminating or reducing its metastatic activity.

P3560Prospects for the use of integrated assessment of gene-candidates polymorphisms in the management of arterial hypertension: let's start

Nowadays a large amount of data about the frequency of gene-candidates polymorphisms occurrence in patients with arterial hypertension (AH) have been accumulated. The using of single polymorphisms for diagnostic and prognostic purposes appeared to be not perspective. However multiple accumulation of gene-candidates polymorphisms in person is realized mostly in formation of AH. The purpose of the research was to compare the proportion of modified gene-candidates in a group of hypertensive patients with a similar group of non-hypertensive patients using the gene modification index (GMI) calculation for possible using in diagnostic and prevention of AH. Methods 180 patients with AH (age 54,2 [43–75], male/female 86/94) and 82 non-hypertensive patients (age 52,6 [42–71], male/female 38/44) were examined (ESC/ISH 2018). For comparative significance in the conducted research the patients under 40 years old were not included. Patients of both groups were perfomed the analysis of polymorphisms of the following candidate genes by PCR: ADD1:1378, AGT: 704, AGT: 521, AGTR1:1166, AGTR2: 1675, CYP11B2:-344, GNB3:825, NOS3:-786, NOS3:894. Then the GMI was formed where the proportion of “pathological” homozygous polymorphism of one gene was 1.5 points, the heterozygous polymorphism – 1 point, “normal” genotype – 0 points. Then points were summed up and formed the GMI as proportion of the “pathological” genotypes, expressed as a percentage. GMI is calculated by the formula: GMI = (N/13,5) × 100, where N is the sum of points of present genetic polymorphisms; N = n1 + n2 + n3 + n4 + n5 + n6 + n7 + n8 + n9; 13,5 – the maximum number of points of present genetic polymorphisms. The GMI from 0 to 20% was considered as low genetic risk, from 21 to 40% – moderate risk, from 41 to 70% – high risk, from 71 to 100% – very high risk. Results In hypertensive patients the low genetic risk was in 5% of cases, in the group of non-hypertensive patients - in 85.4% (p=0.0001); moderate genetic risk was observed in 22.2% of patients with AH and in 13.4% patients without AH (p=0.14); 52.2% of hypertensive patients and 1.2% of non-hypertensive patients had a high genetic risk (p=0.0001); a very high risk was in 20.6% of patients with AH and was absent in patients without AH (p=0.0001). The average mean of GMI in the group with AH was 64.2% [CI 95%, 30–78], in the group of non-hypertensive patients - 22% [CI 95%, 5–30], (p=0.0001). At the same time in GMI less than 25% there was no case of the presence of AH. Conclusions In the conducted research the representative data was obtained: the proportion of the modified gene-candidates significantly exceeded the proportion of the modified genes in non-hypertensive patients. It demonstratively shows the perspectivity of GMI using in the diagnostic and preventive management of patients with AH. GMI up to 25% mostly is not phenotypically realized and the probability of hypertension developing in these patients is extremely low.

Analisis abnormalitas tanaman kelapa sawit (Elaeis guineensis Jacq) hasil kultur jaringan dengan teknik Random Amplified Polymorphic DNA (RAPD) Analysis abnormalities of oil palm (Elaeis guineensis Jacq) from tissue culture by Random Amplified Polymorphic DNA (RAPD

SummaryProblem in oil palm propagation throughtissue culture is the abnormality of reproductiveorgans i.e. female flowers and mantle fruits are inthe same plants or clones. Various abnormalitiesobtained between clones, and could only beidentified after fruit formation. The experimentwas conducted to analyze genetic similarities ofnormal and abnormal genotypes in the same andamong clones, and also to get a specific RAPDband as a marker for abnormalities. Six clones ofoil palm (16 genotypes) of 5-year old MK152,MK203, MK209 and MK212 with normal fruits,female flowers, and abnormal fruits (heavymantled), grown in the field, while two otherclones were MK 104 and MK 176 with normalfruits and heavy mantled. PCR reaction toamplify DNA of 16 genotypes using 15 randomprimers. Genetic similarities and dendogramwere done by NTSYS-pc, while honestly value ofUPGMA analyzed by boostrap with WinBootprogram. The results showed that OPC-07,OPC-09, OPW-19 and SC10-19 were able todetermine the differences of normal andabnormal genotypes in the same clone of sixclones tested. While other primers were onlyable to differentiate between normal andabnormal genotypes only in several clones.Genetic similarities among 16 genotypes testedwere around 0.47-0.96. Genetic similaritiesbetween normal genotype were higher than thatof among abnormal genotypes. MK176 clonewas more stable in culture as compare to otherclones. UPGMA showed that in generaly normalgenotypes and abnormal one, in the sameclones belongs to the same group. The results ofprincipalcomponent analysis showed that from 15primers tested no specific DNA band could beused as a marker for abnormalities. To obtainehave DNA markers, a more sensitive techniquefor DNA analysis is needed.RingkasanMasalah yang dihadapi dalam perbanyakantanaman kelapa sawit dengan teknik kulturjaringan adalah abnormalitas organ reproduktifyaitu terbentuknya bunga jantan dan buah manteldalam klon yang sama. Terjadinya abnormalitassangat beragam, dan teridentifikasi setelahtanaman berbuah. Penelitian ini bertujuan untukmengetahui kesamaan genetik serta penge-lompokan antar genotipe normal dan abnormaldalam klon yang sama maupun antar klon, sertamenetapkan pita DNA penciri untuk abnormalitasdengan RAPD. Enam klon kelapa sawit(16 genotipe) berumur 5 tahun yaitu MK152,MK203, MK209, dan MK212 masing-masingdengan genotipe berbuah normal, berbungajantan, dan berbuah abnormal (mantel berat). Duaklon lainnya yaitu MK104 dan MK176 masing-masing terdiri dari genotipe berbuah normal danmantel berat. Reaksi PCR untuk mengamplifikasiDNA contoh dilakukan menggunakan 15 primeracak. Kesamaan genetik dan pembuatanfenogram dilakukan dengan programNTSYS-pc. Sedang tingkat kepercayaanUPGMA ditetapkan dengan analisisbootstrap menggunakan program WinBoot.Hasil yang diperoleh menunjukkan bahwaprimer OPC-09, SC10-19, OPC-07 danOPW-19 mampu membedakan genotipenormal dan abnormal dalam klon yang samauntuk keenam kon yang diuji. Sedang primerlainnya hanya mampu menunjukkanperbedaan antar genotipe normal danabnormal dalam beberapa klon saja.Kesamaan genetik antar 16 genotipe yangdiuji berkisar antara 0,47-0,96. Kesamaangenetik antar genotipe normal lebih tinggidibandingkan dengan kesamaan genetikantar genotipe abnormal. Klon MK176lebih stabil dalam kultur dibandingkandengan klon lainnya. UPGMA menunjukkanbahwa umumnya genotipe normal danabnormal dalam klon yang sama beradadalam satu grup. Hasil analisis komponenutama menunjukkan bahwa dari 15 primeryang diuji belum mampu menghasilkan pitaDNA penciri untuk abnormalitas. Untukmendapatkan pita DNA penciri, perludilakukan analisis DNA dengan teknik yanglebih sensitif untuk mendeteksi perubahansatu basa oligonukleotida

Analisis abnormalitas tanaman kelapa sawit (Elaeis guineensis Jacq) hasil kultur jaringan dengan teknik Random Amplified Polymorphic DNA (RAPD) Analysis abnormalities of oil palm (Elaeis guineensis Jacq) from tissue culture by Random Amplified Polymorphic DNA (RAPD

SummaryProblem in oil palm propagation throughtissue culture is the abnormality of reproductiveorgans i.e. female flowers and mantle fruits are inthe same plants or clones. Various abnormalitiesobtained between clones, and could only beidentified after fruit formation. The experimentwas conducted to analyze genetic similarities ofnormal and abnormal genotypes in the same andamong clones, and also to get a specific RAPDband as a marker for abnormalities. Six clones ofoil palm (16 genotypes) of 5-year old MK152,MK203, MK209 and MK212 with normal fruits,female flowers, and abnormal fruits (heavymantled), grown in the field, while two otherclones were MK 104 and MK 176 with normalfruits and heavy mantled. PCR reaction toamplify DNA of 16 genotypes using 15 randomprimers. Genetic similarities and dendogramwere done by NTSYS-pc, while honestly value ofUPGMA analyzed by boostrap with WinBootprogram. The results showed that OPC-07,OPC-09, OPW-19 and SC10-19 were able todetermine the differences of normal andabnormal genotypes in the same clone of sixclones tested. While other primers were onlyable to differentiate between normal andabnormal genotypes only in several clones.Genetic similarities among 16 genotypes testedwere around 0.47-0.96. Genetic similaritiesbetween normal genotype were higher than thatof among abnormal genotypes. MK176 clonewas more stable in culture as compare to otherclones. UPGMA showed that in generaly normalgenotypes and abnormal one, in the sameclones belongs to the same group. The results ofprincipalcomponent analysis showed that from 15primers tested no specific DNA band could beused as a marker for abnormalities. To obtainehave DNA markers, a more sensitive techniquefor DNA analysis is needed.RingkasanMasalah yang dihadapi dalam perbanyakantanaman kelapa sawit dengan teknik kulturjaringan adalah abnormalitas organ reproduktifyaitu terbentuknya bunga jantan dan buah manteldalam klon yang sama. Terjadinya abnormalitassangat beragam, dan teridentifikasi setelahtanaman berbuah. Penelitian ini bertujuan untukmengetahui kesamaan genetik serta penge-lompokan antar genotipe normal dan abnormaldalam klon yang sama maupun antar klon, sertamenetapkan pita DNA penciri untuk abnormalitasdengan RAPD. Enam klon kelapa sawit(16 genotipe) berumur 5 tahun yaitu MK152,MK203, MK209, dan MK212 masing-masingdengan genotipe berbuah normal, berbungajantan, dan berbuah abnormal (mantel berat). Duaklon lainnya yaitu MK104 dan MK176 masing-masing terdiri dari genotipe berbuah normal danmantel berat. Reaksi PCR untuk mengamplifikasiDNA contoh dilakukan menggunakan 15 primeracak. Kesamaan genetik dan pembuatanfenogram dilakukan dengan programNTSYS-pc. Sedang tingkat kepercayaanUPGMA ditetapkan dengan analisisbootstrap menggunakan program WinBoot.Hasil yang diperoleh menunjukkan bahwaprimer OPC-09, SC10-19, OPC-07 danOPW-19 mampu membedakan genotipenormal dan abnormal dalam klon yang samauntuk keenam kon yang diuji. Sedang primerlainnya hanya mampu menunjukkanperbedaan antar genotipe normal danabnormal dalam beberapa klon saja.Kesamaan genetik antar 16 genotipe yangdiuji berkisar antara 0,47-0,96. Kesamaangenetik antar genotipe normal lebih tinggidibandingkan dengan kesamaan genetikantar genotipe abnormal. Klon MK176lebih stabil dalam kultur dibandingkandengan klon lainnya. UPGMA menunjukkanbahwa umumnya genotipe normal danabnormal dalam klon yang sama beradadalam satu grup. Hasil analisis komponenutama menunjukkan bahwa dari 15 primeryang diuji belum mampu menghasilkan pitaDNA penciri untuk abnormalitas. Untukmendapatkan pita DNA penciri, perludilakukan analisis DNA dengan teknik yanglebih sensitif untuk mendeteksi perubahansatu basa oligonukleotida

Interrelation of KIF3A gene polymorphism with predisposition to dermatoses

Aim. To study interrelation of KIF3A gene rs2897442 A/G polymorphism with the dermatoses risk in the Republic of Tatarstan. Methods. The study involved 95 dermatological patients (67 patients with atopic dermatitis, 16 - psoriasis, 16 - eczema). The control group included 325 people who have not been diagnosed abovementioned skin diseases. KIF3A gene polymorphism was detected by real time polymerase chain reaction. Clinical examination included the atopic dermatitis diagnosis according to Hanifin and Rajka criteria, disease severity determination according to SCORAD scale, skin structural parameters (microrelief, microtopography) study, skin microbial flora characterization. Results. A statistically significant difference was found out in the KIF3A gene risk allele (G) frequency in patients with skin diseases and concomitant bacterial or fungal infection compared to the control group (57.5 vs 39.7%, p=0.0493). Herewith the presence of unfavourable genotypes (AG+GG) increased the risk of such complications by more than 5 times (OR=5.3, p=0.0145) compared to the normal genotype (AA). Besides, lower (29.2%, p=0.0039) KIF3A gene G allele frequency in the European control group compared with the Russian control group was found. Conclusion. KIF3A gene rs2897442 A/G polymorphism is associated with complicated forms of dermatoses among Republic of Tatarstan residents; population of the Republic of Tatarstan is genetically more prone to the atopic dermatitis development compared to the European population.

Polymorphism of UGT1A1 and Frequency of Hyperbilirubinemia in Patients with Chronic Myeloid Leukemia Treated By Nilotinib

Background. Isolated hyperbilirubinemia mostly of indirect bilirubin fraction is diagnosed in patients with polymorphism of UGT1A1 gene (Gilbert's syndrome), mainly homozygous genotype (TA)7/(TA)7 which encodes the enzyme uridinediphosphoglycosyltransferase 1 (UDP-GT) in hepatocytes. Hyperbilirubinemia is also frequent laboratory abnormality in chronic myeloid (CML) patients treated by nilotinib. Connection of hyperbilirubinemia with UGT1A1 polymorphism in CML patients on nilotinib therapy requires understanding and studying. Aims. To estimate the correlation between polymorphism of UGT1A1 gene and frequency of hyperbilirubinemia in patients with CML treated by nilotinib. Methods. We estimated biochemical parameters in a group of 100 patients treated by nilotinib: bilirubin, transaminases (AST, ALT), persistence of hyperbilirubinemia and biochemical parameters normalization. We also considered patients’ anamnesis for hepatitis and estimated those laboratory abnormalities in previous imatinib therapy as 98 of 100 patients received nilotinib second line after imatinib. Me time of observation on nilotinib therapy was 36.7 months (range 1 – 94.5). Men/women ratio was 45/55. Promoter region of the UGT1A1 gene was studied by allele specific polymerase chain reaction (AS-PCR). Results. Hyperbilirubinemia due to the indirect bilirubin fraction was observed in 84 (84%) of 100 patients. Of those 84 patients hyperbilirubinemia grade 1 was in 41 (49%), grade 2 in 33 (39%), grade 3 in 10 (12%). Normal genotype (TA)6/(TA)6 was in 71 (71%) patients, heterozygous genotype (TA)6/(TA)7 in 19 (19%), homozygous genotype (TA)7/(TA)7 in 10 (10%) patients. Frequency of hyperbilirubinemia grade 1-3 in patients depending on genotype is presented in table1. Figure 1 Figure 1. Hyperbilirubinemia grade 1 was associated mostly with normal genotype patients, grade 2 with normal and abnormal genotype, grade 3 with abnormal and homozygous genotype (9 of 10 patients). In 1 patient with normal genotype grade 3 hyperbilirubinemia was due to intracellular hemolysis approved by laboratory tests. One patient with heterozygous form (TA6/TA7) and normal bilirubin was on nilotinib <1 month. Hyperbilirubinemia on previous imatinib treatment was in 29 (35,7%) of 82 patients with second line nilotinib: grade 1 in 25 (86.2%) of 29 patients (homozygous genotype TA7/TA7 in 5 of 25), grade 2 in 4 (13.8%) of 29 patients (all with homozygous genotype TA7/TA7). Normal bilirubin levels were in 55(46,3%) of 82 patients on previous imatinib therapy. One patient with TA7/TA7 genotype received nilotinib as first line. Bilirubin levels normalized in 48 (57.2%) of 84 patients during 1 to 3 months and persisted in 36 (42.8%). In 8(9,5%) of 84 patients transient ALT and AST elevation was observed: grade 1(1), grade 2 (5) grade 3-4(2); it was resolved and only isolated hyperbilirubinemia was observed later on. In 2 of 84 patients hepatitis C was diagnosed. No treatment discontinuation was done due to hyperbilirubinemia. Summary/Conclusion. In CML patients on nilotinib treatment Grade 3 hyperbilirubinemia as well as previous history of hyperbilirubinemia any grade on imatinib can be a sign of homozygous genotype TA7/TA7. Lower grades of hyperbilirubinemia occur both in patients with normal and abnormal heterozygous genotype. Other reasons for hyperbilirubinemia (hemolysis, hepatitis) should be assessed. No connection of UGT1A1 polymorphism and transaminase (ALT,AST) elevation was established. Disclosures Chelysheva: Bristol-Myers Squibb: Consultancy, Honoraria; Novartis International AG: Consultancy, Honoraria. Turkina:Bristol-Myers Squibb: Consultancy, Honoraria; Novartis International AG: Consultancy, Honoraria.

Maternal/newborn genotype contribution of the renin–angiotensin system (Met235Thr, Thr174Met, I/D-ACE, A2350G-ACE, A1166C-AT2R1, C3123A- AT2R2, 83A/G-REN) to the risk of pre-eclampsia: a Romanian study

Introduction: We evaluated the association of the mutated genotypes Met235Thr-AGT, Thr174Met-AGT, I/D-ACE, A2350G-ACE, A1166C-AT2R1, C3123A-AT2R2, 83A/G-REN with the risk and outcome of pre-eclampsia; we also investigated whether genes in newborns increase maternal risk of pre-eclampsia. Materials and methods: Thirty-six pairs of pre-eclamptic women and their newborns were genotyped, along with 71 pairs of controls (mothers/newborns) using PCR-RFLP analysis. Results: The Thr235/Thr235 (OR 3.44, p = 0.01), DD (OR 2.66, p = 0.039), CC1166 (OR 5.56, p = 0.04), AA3123 (OR 3.77, p = 0.03) and GG83 (OR 8.32, p = 0.006) genotypes are significantly associated with pre-eclampsia. Women with pre-eclampsia positive for Met235Thr (34.64 ± 3.92 weeks vs. 38 ± 2 weeks), Thr174Met (32.58 ± 3.92 weeks vs. 36.38 ± 3.25 weeks), I/D (34.47 ± 3.67 weeks vs. 38.33 ± 3.5 weeks) delivered at a significant lower gestational age compared with pre-eclamptic women with a normal genotype. Newborns from women with pre-eclampsia positive for Thr174Met (2190 ± 820.21 g vs. 2702.08 ± 967.23 g), I/D (2399.33 ± 938.38 g vs. 3191.66 ± 684.40 g) had a significant lower birth weight compared with newborns from women with normal pregnancies. When both the mother and the newborn were positive for Met235Thr, I/D, A2350G, A1166C or 83A/G polymorphisms, the risk for pre-eclampsia was significantly increased at 6.67 ( p < 0.01), 5 ( p < 0.01), 3.33 ( p = 0.006), 2.72 ( p = 0.04) and 7.8 ( p < 0.01), respectively. Conclusions: The results of our study confirm that, in pre-eclampsia, both maternal and newborn genetic variations implicated in blood pressure regulation are important.

Chemical composition and in situ ruminal nutrient degradability of normal and brown midrib forage pearl millet grown in southwestern Québec

The objective of this study was to determine the chemical composition and in situ ruminal degradability of normal and brown midrib (bmr) forage pearl millet [Pennisetum glaucum (L.) R. Br.] grown in southwestern Québec conditions. Forage was harvested twice during the season. Relative to normal genotype, bmr millet contained less (P < 0.05) neutral detergent fiber (NDF) and acid detergent lignin and more (P < 0.05) crude protein (CP). Fiber fractions were similar for the two harvests. However, CP content was higher (P < 0.05) in the first than the second harvest. In situ ruminal degradabilities of DM, CP and NDF were all higher (P < 0.05) for bmr than normal forage millet and were not affected by harvest. Key words: Forage quality, pearl millet, ruminal degradability, protein fractions, brown midrib