Indenture between Samuel D. Woodruff and Lewis Better

Indenture regarding articles of agreement between Samuel D. Woodruff of St. Catharines and Lewis Better of the Township of Gainsborough for lot no. 3 in the township of Gainsborough, Apr. 23, 1896.

Indenture between Samuel D. Woodruff and Jane Caroline Woodruff and Hamilton Killaly Woodruff

Indenture between Samuel D. Woodruff and Jane Caroline Woodruff and Hamilton Killaly Woodruff in which Samuel Woodruff signed over pew 15 in St. George’s Church, St. Catharines to Hamilton Killaly Woodruff for $1.00, May 12, 1900.

The letter is addressed to Samuel D. Woodruff and is signed by Thomas Steers

Letter which is very stained, fragile and has holes in it. Text is partially illegible and faded. The letter is addressed to Samuel D. Woodruff and is signed by Thomas Steers. It is written in ink, but someone has added comments in pencil. It regards Richard and William Woodruff. There are questions on the document which include: “Has M. Clement died interstate?” [in pencil – “he has”]; “Has he an heir at law other than” [the rest is faded, someone has written in pencil “he has, Richard and William Woodruff”], March 23, 1847.

Indenture of Agreement for Sale of Land between S.D. Woodruff and Elizabeth Cudney

Indenture of agreement for Sale of Land between S.D. Woodruff of St. Catharines and Elizabeth Cudney of Willoughby regarding a footpath and Lots 9 and 10 in Willoughby, Feb. 6, 1893.

Indenture of memorandum of an agreement between S.D. Woodruff and James L. Burton and M. Burton

Indenture of memorandum of an agreement between S.D. Woodruff of St. Catharines and James L. Burton and M. Burton, both of Barrie, trading under the name of Burton and Bro. that Burton and Bro. would buy all the pine timber located in berths 192 and 198. Burton and Bro. agrees to have all timber cut. The agreement is signed by S.D. Woodruff and Burton and Bro. This document is badly burned along the left hand side. This does not affect the text, July 11, 1877.

Agreement between S.D. Woodruff and Nathaniel Dyment of Barrie

Agreement between S.D. Woodruff and Nathaniel Dyment of Barrie. S.D. Woodruff is the owner of license no. 198 of season 1877/78 for berth no. 198. S.D. Woodruff has agreed to sell this license, Nov. 23, 1877.

Letter is addressed to S.D. Woodruff and is from Dunnville [signature illegible]

Letter is addressed to S.D. Woodruff and is from Dunnville [signature illegible] (3 pages, handwritten). The writer suggests that the head of the Welland Canal should be guarded. He has made a deal with the Sappers and Miners [Corps of Royal Military Artificers, consisting of noncommissioned officers and privates] to be stationed at this point, Jan.24, 1862.

List which includes costs, plans and receipts for amounts received between S.D. Woodruff and Boyd and Schurr

List (8 pages, handwritten) which includes costs, plans and receipts for amounts received between S.D. Woodruff and Boyd and Schurr, Dec. 3, 1875.

Flyer about railroad bonds from E.D. Shepard and Co. Bankers

Flyer (2 double sided pages, printed) about railroad bonds from E.D. Shepard and Co. Bankers, New York, n.d.

Decreased GABAA Receptors Functional Regulation 3 in the Cerebral Cortex and Brainstem of Hypoxic Neonatal Rats: 4 Effect of Glucose and Oxygen Supplementation

Hypoxia in neonates can lead to biochemical and molecular alterations mediated through changes in neurotransmitters resulting in permanent damage to brain. In this study, we evaluated the changes in the receptor status of GABAA in the cerebral cortex and brainstem of hypoxic neonatal rats and hypoxic rats supplemented with glucose and oxygen using binding assays and gene expression of GABAAa1 and GABAAc5. In the cerebral cortex and brainstem of hypoxic neonatal rats, a significant decrease in GABAA receptors was observed, which accounts for the respiratory inhibition. Hypoxic rats sup- plemented with glucose alone and with glucose and oxygen showed, respectively, a reversal of the GABAA receptors, andGABAAa1 and GABAAc5 gene expression to control. Glucose acts as an immediate energy source thereby reducing the ATP-depletion-induced increase in GABA and oxygenation, which helps in encountering anoxia. Resuscitation with oxygen alone was less effective in reversing the receptor alterations. Thus, the results of this study suggest that reduction in the GABAA receptors functional regulation during hypoxia plays an important role in mediating the brain damage. Glucose alone and glucose and oxygen supplementation to hypoxic neonatal rats helps in protecting the brain from severe hypoxic damage.

Effect of prolonged intravenous glucose and essential amino acid infusion on nitrogen balance, muscle protein degradation and ubiquitin-conjugating enzyme gene expression in calves

Background: Intravenous infusions of glucose and amino acids increase both nitrogen balance and muscle accretion. We hypothesised that co-infusion of glucose ( to stimulate insulin) and essential amino acids (EAA) would act additively to improve nitrogen balance by decreasing muscle protein degradation in association with alterations in muscle expression of components of the ubiquitin-proteasome proteolytic pathway. Methods: We examined the effect of a 5 day intravenous infusions of saline, glucose, EAA and glucose + EAA, on urinary nitrogen excretion and muscle protein degradation. We carried out the study in 6 restrained calves since ruminants offer the advantage that muscle protein degradation can be assessed by excretion of 3 methyl-histidine and multiple muscle biopsies can be taken from the same animal. On the final day of infusion blood samples were taken for hormone and metabolite measurement and muscle biopsies for expression of ubiquitin, the 14-kDa E2 ubiquitin conjugating enzyme, and proteasome sub-units C2 and C8. Results: On day 5 of glucose infusion, plasma glucose, insulin and IGF-1 concentrations were increased while urea nitrogen excretion and myofibrillar protein degradation was decreased. Co-infusion of glucose + EAA prevented the loss of urinary nitrogen observed with EAA infusions alone and enhanced the increase in plasma IGF-1 concentration but there was no synergistic effect of glucose + EAA on the decrease in myofibrillar protein degradation. Muscle mRNA expression of the ubiquitin conjugating enzyme, 14-kDa E2 and proteasome sub-unit C2 were significantly decreased, after glucose but not amino acid infusions, and there was no further response to the combined infusions of glucose + EAA. Conclusion: Prolonged glucose infusion decreases myofibrillar protein degradation, prevents the excretion of infused EAA, and acts additively with EAA to increase plasma IGF-1 and improve net nitrogen balance. There was no evidence of synergistic effects between glucose + EAA infusion on muscle protein degradation or expression of components of the ubiquitin-proteasome proteolytic pathway.

Acute effects of meal fatty acids on postprandial NEFA, glucose and apo E response: implications for insulin sensitivity and lipoprotein regulation?

Our aim was to determine whether meal fatty acids influence insulin and glucose responses to mixed meals and whether these effects can be explained by variations in postprandial NEFA and Apo, which regulate the metabolism of triacylglycerol-rich lipoproteins (Apo C and E). A single-blind crossover study examined the effects of single meals enriched in saturated fatty acids SFA), n-6 PUFA and MUFA on plasma metabolite and insulin responses. The triacylglycerol response following the PUFA meal showed a lower net incremental area under the curve than following the SFA and MUFA meals (P < 0.007). Compared with the SFA meal, the PUFA meal showed a lower net incremental area under the curve for the NEFA response from initial suppression to the end of the postprandial period (180-480 min; P < 0.02), and both PUFA and MUFA showed a lower net incremental glucose response (P < 0.02), although insulin concentrations were similar between meals. The pattern of the Apo E response was also different following the SFA meal (P < 0.02). There was a significant association between the net incremental NEFA (180-480 min) and glucose response (r(s)=0.409, P=0.025), and in multiple regression analysis the NEFA response accounted for 24 % of the variation in glucose response. Meal SFA have adverse effects on the postprandial glucose response that may be due to greater elevations in NEFA arising from differences in the metabolism of SFA- v. PUFA- and MUFA-rich lipoproteins. Elevated Apo E responses to high-SFA meals may have important implications for the hepatic metabolism of triacylglycerol-rich lipoproteins.