We describe the establishment and current content of the ImmuneCODE™ database, which includes hundreds of millions of T-cell Receptor (TCR) sequences from over 1,400 subjects exposed to or infected with the SARS-CoV-2 virus, as well as over 135,000 high-confidence SARS-CoV-2-specific TCRs. This database is made freely available, and the data contained in it can be downloaded and analyzed online or offline to assist with the global efforts to understand the immune response to the SARS-CoV-2 virus and develop new interventions.

This study examined the anaerobic and aerobic contributions to muscle metabolism during high intensity short duration exercise. Six males [mean (SD): age 25.0 (6.0) years, height 179.0 (8.2) cm, mass 70.01 (7.42) kg, VO2max 4.63 (0.53) l.min-1, body fat 12.7 (2.3)%] performed three counterbalanced treatments of 30, 60 and 90 s of maximal cycling on an air-braked ergometer. All treatments were also performed on days when biopsies were not taken from the vastus lateralis muscle and cannulae not inserted into a forearm vein to ascertain whether these procedures adversely affected performance. The mean results can be summarised as follows: (Table: see text). The muscle lactate and O2 deficit data suggested that 60 and 90 s were more appropriate durations than 30 s for assessing the anaerobic capacity on an air-braked cycle ergometer. The mean power outputs also indicated that the invasive procedures did not adversely affect performance [corrected].

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This report adds 4 members in a kindred with diabetes insipidus, diabetes mellitus, and optic atrophy to the published descriptions (DeLawter, 1949;Fraccaro and Gastaldi, 1952;Casa, 1955;Raiti, Plotkin, and Newns, 1963;Bretz et al, 1970;Ikkos et al, 1970) left frontal area and right anterior temporal spiking. Audiometry demonstrated moderate bilateral perception deafness. Craniotomy performed at age 11 revealed arachnoiditis in the area of the optic chiasm with atrophy of both optic nerves.At age 21, the patient was 167 cm tall and weighed 66-7 kg. In addition to the primary optic atrophy, vertical nystagmus and rare microaneurysms were present. Knee and ankle tendon reflexes could not be obtained. His testis was 4 cm long on the right and 3-5 cm on the left.Except for variable hyperglycaemia, blood and serum solutes have been normal. Glucose tolerance test revealed a clearly diabetic curve with no evidence of insulin response (Morgan, 1966) to an oral glucose load. A minor growth hormone (Morgan, 1966) peak was recorded at the 5th hour of this test. Plasma ll(OH) corticosteroid levels (Mattingly, 1962) have been within the normal range. Intravenous arginine (0-41 mg/kg) had no effect upon serum insulin levels but did produce a rise in serum growth hormone to 11 ng/ml. Serum PBI (Danowski, Johnston, and Greenman, 1950) and thyroidal 13"I uptake were 3-8y% and 16%, respectively.Creatinine clearance (Peters, 1942) was 141 ml/min. The urinary 17-ketosteroids (Holtorff and Koch, 1940) were 12-2 with Porter-Silber chromogens (Porter and Silber, 1950) at 11-4 and compound S metabolites (Henke, Doe, andJacobson, 1960) at 0-88 mg/day. Case 2. (brother of case 1). This 24-year old single male was found to have diabetes mellitus at the age of 3 years following polyuria, polyphagia, and polydipsia. He was treated with an anti-diabetic diet and insulin, most recently 54 units of NPH daily. At the age of 12 years, a diagnosis of optic atrophy was also made following the discovery of optic atrophy in his sibs. At age 15, urine volumes increased to 8 1/dy. Twenty hours of water deprivation raised urine osmolarity relative to serum only slightly, ie, 455 versus 314 milliosmols, respectively, during an interval when urine sugar was zero. Chlorpropamide, 250 mg/dy, reduced urine volumes to 21/dy. The intravenous infusion of arginine (0-41 mg/kg) produced a rise in the serum growth hormone to 25 ng/ml. 408 on 11 May 2018 by guest. Protected by copyright.

In 707 non-obese female adults with unimpaired glucose tolerance, the fasting blood glucose levels of those in the fourth, fifth and sixth decades of life exceeded the levels found in those of the third decade (20-29 years), but there was no evidence of a progressive increase in successive age decades. The slightly greater fasting glycemia in the later age decades was accompanied by higher increments in blood glucose in the first half hour of the glucose tolerance test. These higher levels of glucose during the fasting state and in the first half hour after oral administration of glucose were not associated with increments in serum insulin greater than those recorded for the third age decade. This age-related increase in fasting and post-glucose blood sugar levels without an increase in serum insulin could result from the age-related increase in the thickness of capillary basement membranes. The higher levels of glucose could then serve to restore glucose transport and cell glucose metabolites to normal without evoking a rise in serum insulin.In 479 obese women with unimpaired glucose tolerance, there was no evidence of the age-related increase in fasting blood glucose nor the slightly exaggerated hyperglycemia found early in the test in non-obese subjects with normal glucose tolerance. The relative fasting hyperinsulinemia and the increased insulin responses to induced hyperglycemia known to characterize obese persons were present in all age decades but the hyperinsulinemia was less marked in subjects older than 30. In these obese subjects with unimpaired glucose tolerance, there was no evidence of any delay in the insulin response to the induced hyperglycemia.In a previous study (1), we observed that in older non-obese females with unimpaired glucose tolerance there was a slightly higher concentration of fasting blood glucose and a slightly greater blood glucose response without 1na a concomitant increase in the serum insulin level. In the studies reported here, we characterize the glucose and insulin patterns for successive age decades in both non-obese and obese women. Detailed analyses of the data indicate that, within the range of normal glucose tolerance, only minor age-related differences are evident in the blood sugar and insulin responses to orally administered carbohydrate. However, the many incompletely defined aspects of aging and of obesity warrant citation of even slight differences which are lost when such data are pooled solely on the basi~of age or body weight.

Hyperinsulinemic patterns are a well recognized feature of equivocal glucose tolerances of the chemical diabetes type, i.e. those that are neither definitely nondiabetic nor clearly diabetic. A more complete characterization of such insulin responses is obtained when the data are expressed in terms of increments in insulin from the zero time point.Thus, two patterns of insulin increments after oral glucose become evident when the equivocal zone of glucose tolerance is divided into lower and upper segments. Tests in the lower segment show normal increments at the halfhour point of the test; at one hour these tests show excessive increments which persist throughout the five hours of observation. On the other hand, tests in the upper zone show delays in the serum insulin rise at the half-hour point, followed by normal increments at one hour and excessive increments thereafter. The pattern is the same whether or not obesity is present. It is suggested that tests in the equivocal zone of Glucose Tolerance Sum values be taken to be indicative of chemical diabetes. Tests with the Sum in the lower half of the equivocal zone could then represent chemical diabetes with mild intolerance stemming from insulin ineffectiveness, since insulin increments in this group are at or above the mean values recorded in nondiabetic controls. On the other hand, chemical diabetes with moderate glucose intolerance and Glucose Tolerance Sums in the upper half of the equivocal zone would be understood to result from a combination of an initial delay in the serum insulin rise followed by normal and then excessive increments in serum insulin with the latter two indicative of insulin ineffectiveness. However, insulin ineffectiveness may also be present at the time of the insulin delay.High glucose:insulin ratios in tests indicative of chemical diabetes are almost always attributable to higher glucose increments with insulin increments normal or excessive compared to normal glucose tolerances. Deficient insulin increments contribute to the high ratios only at the half-hour point in tests with Glucose Tolerance Sums in the upper zone of equivocal glucose tolerances. DIABETES 22:808-12, November, 1973.