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Biomedical subjects

D L Cook

Publications and source records attributed to D L Cook.

66 records · Page 4Linked to original sources

Intraoperative decision making in the treatment of shoulder instability.

Between April 1990 and April 1994, 100 patients with a preoperative diagnosis of anterior instability underwent a diagnostic arthroscopy of the shoulder. Patients with isolated SLAP lesions were excluded from the study. Patients with multidirectional instability, bony Bankart lesions, and large Hill-Sachs lesions were also excluded. Football players and dominant arm throwing athletes were also excluded. Thirty patients remained who had post-traumatic, unidirectional, anterior instability and a repairable Bankart lesion and did not have any exclusions as noted above. All of these patients underwent an initial attempt at an arthroscopic Sure-Tac stabilization (Smith & Nephew, Andover, MA). Twenty-three patients met our criteria for a secure fixation but 7 did not. These 7 underwent an immediate arthrotomy and open Bankart repair. All of the patients were available at follow-up at an average of 47 months (range, 36 to 72 months). The patients were evaluated by the Rowe shoulder rating scale. There have been two cases of recurrent subluxation and one case of recurrent dislocation in the Sure-Tac group. All three occurred over 2 years later. All three had recurrent Bankart lesions and underwent an arthrotomy and Bankart repair. There were no cases of recurrence of subluxation or dislocation in our initial open Bankart repair group. Sure-Tac arthroscopic anterior stabilization of the shoulder can initially give good results but these results appear to deteriorate over time and increased activity of the patient. We currently do not recommend a Sure-Tac repair even in a selective group of patients with an isolated Bankart lesion. This is based on our excellent results following an open Bankart repair and a 13% recurrence rate following Sure-Tac stabilization in carefully selected patients.

Adult↗

Lowering of pHi inhibits Ca2+-activated K+ channels in pancreatic B-cells.

Glucose-dependent periodic electrical activity of membranes of pancreatic islet cells mediates calcium uptake, which is important for glucose-induced insulin release. As yet there has been no direct evidence identifying the 'second messenger' which couples the uptake and metabolism of glucose to the change of membrane electrical activity. Recent evidence showing that intracellular acidification stimulates islet B-cell electrical activity in a glucose-like manner has suggested that protons produced metabolically may serve as messengers by blocking K+ channels and depolarizing the membrane. Thus protons have been suggested to inhibit the Ca2+-activated K+-conductance [GK(Ca)] which is thought to produce the 'pacemaker' current responsible for the rhythmic firing of plateau depolarizations and Ca2+ spikes. Although these conductance channels have been characterized at the single channel level in several tissues, little is known of their response to intracellular pH (ref. 19) and they have not yet been characterized in B-cells. We have, therefore, used the patch-clamp method to study identified rat B-cells and show here that the B-cell GK(Ca) channel is activated by membrane depolarization as well as by cytoplasmic Ca2+, while it is inhibited by acidification of the cytoplasmic membrane surface.

Animals↗

Intracellular ATP directly blocks K+ channels in pancreatic B-cells.

It is known that glucose-induced depolarization of pancreatic B-cells is due to reduced membrane K+-permeability and is coupled to an increase in the rate of glycolysis, but there has been no direct evidence linking specific metabolic processes or products to the closing of membrane K+ channels. During patch-clamp studies of proton inhibition of Ca2+-activated K+ channels [GK(Ca)] in B-cells, we identified a second K+-selective channel which is rapidly and reversibly inhibited by ATP applied to the cytoplasmic surface of the membrane. This channel is spontaneously active in excised patches and frequently coexists with GK(Ca) channels yet is insensitive to membrane potential and to intracellular free Ca2+ and pH. Blocking of the channel is ATP-specific and appears not to require metabolism of the ATP. This ATP-sensitive K+ channel [GK(ATP)] may be a link between metabolism and membrane K+-permeability in pancreatic B-cells.

Adenosine Triphosphate↗

The impact of a diabetes nurse educator on nurses' knowledge of diabetes and nursing interventions in a home care setting.

The purpose of this study was to compare nurses' knowledge of diabetes and nursing interventions in a home health care agency (HHCA) that employed a diabetes nurse educator (DNE) and an agency that did not employ a DNE. Nurse knowledge of diabetes mellitus was measured using the Diabetes: Basic Knowledge Test (DBKT). Nursing care interventions for patients with diabetes were measured using a researcher-developed tool, the Nursing Care Intervention Tool (NCIT). The data analysis showed that the nurses in the agency with the diabetes nurse educator were significantly more knowledgeable about diabetes. The data also showed that the nurses in the HHCA with a diabetes nurse educator provided a significantly higher standard of patient care than the nurses in the agency without a diabetes nurse educator.

Diabetes Mellitus↗

Autonomic neural dysfunction in recently diagnosed diabetic subjects.

Because onset of autonomic neural dysfunction in the diabetic syndrome has not been well established, sensitive and quantitative measures of autonomic nervous system (ANS) function were made in 19 non-insulin-dependent (NIDD) and 14 insulin-dependent (IDD) recent-onset diabetic subjects. The known duration of diabetes mellitus in the NIDD subjects was less than or equal to 12 mo. The duration in the IDD subjects was less than or equal to 24 mo. RR-variation during beta adrenergic blockade (an index of an ANS reflex involving the cardiac parasympathetic nervous system [PNS] pathway) was smaller than that of control subjects in both NIDD (P less than 0.001) and IDD subjects (P less than 0.01). This PNS abnormality was not likely to be due to volume depletion since acute volume depletion induced by furosemide in six normal subjects (1608 +/- 105 ml, mean +/- SEM) did not change RR-variation. Dark-adapted pupil size after topical PNS blockade (an index of iris sympathetic nervous system [SNS] activity) was also smaller in both groups of diabetic subjects (NIDD, P less than 0.01; IDD, P less than 0.05). Pupillary latency time (an index of an ANS reflex involving iris PNS pathway) was prolonged in the NIDD subjects (P less than 0.005) but was not significantly altered in the IDD subjects. Thus, it would appear that the ANS is impaired soon after the diagnosis of diabetes mellitus. We hypothesize that early impairment of the ANS is common in IDD and NIDD subjects. This finding is consistent with the hypothesis that abnormal carbohydrate metabolism is an important factor in the etiology of diabetic autonomic neuropathy.

Adult↗

Correlations among autonomic, sensory, and motor neural function tests in untreated non-insulin-dependent diabetic individuals.

A well-defined group of untreated non-insulin-dependent (NIDD) subjects were evaluated to determine whether involvement of neural function measurements is generalized and symmetrical and to compare the autonomic, sensory, and motor neural measurements. After age adjustment, the sensory and motor neural function measurements were significantly slower in the diabetic group than in normal subjects (P less than 0.01). Similarly, the autonomic nervous system function measurements were also abnormal in the NIDD group (P less than 0.01). Further analysis revealed that each of the specific measurements--median motor nerve conduction velocity (NCV,P less than 0.005), peroneal motor NCV (P less than 0.005), median sensory NCV (P less than 0.005), dark-adapted pupil size after muscarinic blockade (P less than 0.02), pupillary latency time (P less than 0.02), and RR-variation after beta adrenergic blockade (P less than 0.001)--was significantly less by analysis of covariance after age adjustment in the NIDD group than in normal subjects. Thus, there was evidence of motor and sensory neural impairment in the upper and lower extremities as well as evidence of impairment of the reflex arcs involving the parasympathetic nerves to the heart and eye and the sympathetic nerves to the iris. Further analysis revealed that right and left NCV were correlated (P less than 0.01), as were the median motor and median sensory NCV (P less than 0.01), the median motor and peroneal motor NCV (P less than 0.001), and the peroneal motor and median sensory NCV (P less than 0.001). Thus, there was evidence of symmetrical upper and lower limb, as well as motor and sensory proportional involvement of large nerve fiber NCV in this group of NIDD subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The biological properties of aspartame. II. Actions involving the gastrointestinal system.

Aspartame (APM) was investigated in several pharmacological tests to delineate any effects on the gastrointestinal system. The compound did not affect food consumption at one hour following a single intragastric dose of 200 mg/kg in rats. There was no evidence of inhibition or stimulation of the gastric juice secretion rate, the concentration of gastric acid, acid output or proteolytic activity following an intragastric dose of 250 mg/kg in five-hour pylorus-ligated rats. Likewise, APM at the same dosage did not significantly affect gastric ulceration induced by nineteen hours of pylorus-ligation. In several in vitro tests it was demonstrated that APM did not affect the proteolytic activity of pepsin or the lipolytic activity of pancreatic lipase at concentrations of 143 microgram and 1.25 mg/ml, respectively. Its anticholinergic activity was found to be insignificant, less than 0.001 times the potency of atropine sulfate, when measured against acetylcholine-induced contraction of isolated rabbit ileum. These data indicate that APM may be devoid of undesirable side effects on the gastrointestinal tract when used as a food sweetening agent.

Acetylcholine↗