Biomedical subjects
Publications and source records attributed to G Capasso.
Four patients who suffered from minimal trauma knee hemarthrosis are presented. In all patients, the cause of the hemarthrosis was not the traumatic event in itself, but an underlying clotting or collagen disorder. The necessity of interaction between the orthopaedic surgeon and a coagulation unit is stressed.
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During their daily surgical activity in Hiv-positive and AIDS patients the authors have seen in surgical treatment of anogenital recurring acuminate condylomata (treated with diatermocoagulation) in 1995 that prescribing elotrimazole ointment in Candida albicans infection of the same regions there was and amelioration or the healing of the mycotic infection but also a net lowering of the condylomata and persistent latency (disease-free time) till to the next local recurrence. So they have hypothesized and antiviral and antiblastic effect of elotrimazole. Under this heading they have done a literature research discovering that in 1995, only some months ago, two fundamental works have been published on this intriguing topic. They demonstrate at an experimental level in mice a strong antiviral and antiblastic activity of clotrimazole. This new fascinating field is completely open to future research and the consequences at a therapeutic level will be of utmost importance.
The role of adrenal steroids in the regulation of bicarbonate absorption in the loop of Henle was studied by in vivo microperfusion. Bicarbonate transport (JHCO3) was measured by microcalorimetry and fluid reabsorption by [14C]inulin, 7-10 days after surgery, in 1) sham-operated control rats, 2) adrenalectomized (Adx) rats, 3) Adx rats receiving dexamethasone (1.2 micrograms.100 g body wt-1.24 h-1) and a low dose of aldosterone (0.5 micrograms.100 g body wt-1.24 h-1), 4) Adx rats receiving dexamethasone, 5) Adx rats receiving a low dose of aldosterone, and 6) Adx rats receiving a high dose of aldosterone (1.0 micrograms.100 g body wt-1.24 h-1). JHCO3 along the loop of Henle was decreased by 40% in Adx rats. JHCO3 was increased by dexamethasone alone and by dexamethasone plus a low dose of aldosterone to rates observed in fully supplemented Adx rats. Aldosterone given alone at a low physiological dose had no effect, but, when administered at a high dose, returned JHCO3 to normal.
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An increase in glomerular filtration rate (GFR) induces adaptive changes in tubular function to prevent the urinary loss of water and electrolytes. This is also true for acid-base balance: the increase in filtered bicarbonate load will stimulate H+ secretion at the level of several segments including the proximal tubule, the loop of Henle, and the distal tubule. There is an activation of both the luminal Na+/H+ exchanger and H(+)-ATPase, and basal-lateral Na(+)-HCO3- cotransport which allows an increase in luminal H+ secretion and basal lateral HCO3- exit. The stimulation of electrolyte reabsorption is very important at the level of the thick ascending limb of Henle, a segment that shows consistent hypertrophy in many models of hyperfiltration. Along this segment, increased Na+ and Cl- reabsorption has been found in rats receiving a high-protein diet. The ensuing reduced Na+ and Cl- concentrations, at the level of the macula densa, could weaken the signal responsible for initiating the tubuloglomerular feedback (TGF), thus allowing GFR to increase.
This article analyzes 57 reports published in the years 1983 through 1964 that addressed the issue of the renal hemodynamic response to an oral protein load. Seventy-three groups are reported in those studies: 52 were healthy subjects (n = 627) and 21 had renal disease (n = 256); 47 were studied using inulin (n = 407 healthy people and 112 renal patients); 26 groups were studied using creatinine (n = 220 healthy people and 144 renal patients). Patients with liver cirrhosis were also analyzed. There was great heterogeneity in methodology used, emphasizing the need for standardization. The role of plasma amino acids, glucagon, insulin, growth hormone, PGE2, 6-ketoPGA1 alpha, brain-gut peptides, ANP, AVP, dopamine, and kinins in promoting the renal hemodynamic response to an oral protein load is discussed.
Chronic peritoneal dialysis (CPD) is the first treatment modality for most infants with end-stage renal failure; this group of patients shows peculiar clinical and technical problems. We present the data from a National Registry on 22 children starting CPD under one year of age, representing 11.6% of the total population of the Registry (189 patients). Mean weight at start of CPD was 6.1 +/- 1.8 kg and duration of dialysis was 22.1 +/- 15.5 months. During the follow-up period, 9 patients were transplanted, 1 was shifted to hemodialysis, and 4 died. Patient survival was 89.1% and 82.2% at 1 and 2 years (97.9% and 96.5% in the group of 167 older children); technique survival results were 89.1% at 1 year and 77.1% at 2 years (vs 92.5% and 85.7%, respectively). The incidence of peritonitis was 1 episode every 15.6 CPD-months (1:16.1 in the older children). Catheter-related complications occurred more frequently in infants (1:11.8 vs 1:17 episode:CPD-months), even if this difference was not statistically significant. Statural growth was on average -0.29 +/- 0.66 SD/year with a significant improvement between the first (-0.50 +/- 0.79) and the second (+0.23 +/- 0.77) year of CPD. Our data confirm that infants represent a higher risk group and that they can be treated satisfactorily with CPD while awaiting renal transplantation.
The loop of Henle (LOH) reabsorbs approximately 15% of filtered HCO3- via a luminal Na(+)-H+ exchanger and H+ATPase. During acute metabolic alkalosis (AMA) induced by i.v. HCO3- infusion, we have observed previously inhibition of LOH net HCO3- reabsorption (JHCO3-), which contributes to urinary elimination of the HCO3- load and correction of the systemic alkalosis. To determine whether the activities of the Na(+)-H+ exchanger and/or H(+)-ATPase are reduced during AMA, two inhibitors believed to be sufficiently specific for each transporter were delivered by in vivo LOH microperfusion during AMA. AMA reduced LOH JHCO3- from 205.0 +/- 10.8 to 96.2 +/- 11.8 pmol.min-1 (P < 0.001). Luminal perfusion with bafilomycin A1 (10(-4) mol.l-1) caused a further reduction in JHCO3- by 83% and ethylisopropylamiloride (EIPA; 5.10(-4) mol.l-1) completely abolished net HCO3- reabsorption. The combination of bafilomycin A1 and EIPA in the luminal perfusate was additive, resulting in net HCO3- secretion (-66.6 +/- 20.8 pmol.min-1; P < 0.001) and abolished net fluid reabsorption (from 5.0 +/- 0.6 during AMA to 0.2 +/- 1.1 nl.min-1; P < 0.001). To establish whether HCO3- secretion via luminal stilbene-sensitive transport mechanism participates in LOH adaptation to AMA, we added diisothiocyanato-2,2'-stilbenedisulphonate (DIDS; 10(-4) mol.l-1) to the perfusate. No effect was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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We assessed the effects of changes in potassium (K+) balance on the function of the loop of Henle by a combination of renal clearance and microperfusion experiments. Rat superficial cortical nephrons were perfused in vivo at 20 nl.min-1 from late proximal to early distal tubule with an artificial end-proximal solution containing either 3.8 or 1.8 mM potassium. Rats were fed a control diet, a low-potassium diet for at least three weeks, or a high-potassium diet for 10 to 14 days. When compared with the appropriate end-proximal potassium concentration in the perfusion fluid, potassium absorption along the loop of Henle (JK) increased in potassium-depletion whereas sodium (JNa) and fluid (Jv) absorption decreased. In rats fed a high-potassium diet, absorption of potassium, sodium and fluid was depressed. We propose that changes of external potassium balance affect the transport of electrolytes and fluid along the loop of Henle in vivo by modulating the transport of potassium and sodium primarily in the thick ascending limb. Changes in potassium reabsorption may also be affected by alterations of potassium-recycling.
Joseph Jacob Plenck (1735-1807) is considered to be the forerunner of modern European dermatology, who also compiled a list of about 800 plants with medicinal uses. Of these about 115 have diuretic properties and are currently included in various pharmacopeias. They were traditionally used to cure ascites of various causes, in urolithiasis, nephritis, cystitis, bladder ulcers, strangury, urinary retention and incontinence. Few of these plants have been fully investigated by modern medicinal chemists, and many are worthy of further study.
The medical history of salt begins in ancient times and is closely related to different aspects of human history. Salt may be extracted from sea water, mineral deposits, surface encrustations, saline lakes and brine springs. In many inland areas, wood was used as a fuel source for evaporation of brine and this practice led to major deafforestation in central Europe. Salt played a central role in the economies of many regions, and is often reflected in place names. Salt was also used as a basis for population censuses and taxation, and salt monopolies were practised in many states. Salt was sometimes implicated in the outbreak of conflict, e.g. the French Revolution and the Indian War of Independence. Salt has also been invested with many cultural and religious meanings, from the ancient Egyptians to the Middle Ages. Man's innate appetite for salt may be related to his evolution from predominantly vegetarian anthropoids, and it is noteworthy that those people who live mainly on protein and milk or who drink salty water do not generally salt their food, whereas those who live mainly on vegetables, rice and cereals use much more salt. Medicinal use tended to emphasize the positive aspects of salt, e.g. prevention of putrefaction, reduction of tissue swelling, treatment of diarrhea. Evidence was also available to ancient peoples of its relationship to fertility, particularly in domestic animals. The history of salt thus represents a unique example for studying the impact of a widely used dietary substance on different important aspects of man's life, including medical philosophy.
The study was devised to establish the role of prostaglandin E2, prostaglandin1 alpha and thromboxane A2 in the genesis of glomerular hyperfiltration response to a meat meal in healthy humans. To this end, a group of 8 healthy women was studied 4 times: in the control state (study 1), after a meat meal (study 2), following a meat meal associated with intravenous aspirin (study 3) and finally after a meat meal associated with intravenous aspirin following 2-day pretreatment with oral aspirin (study 4). Urinary excretion of prostaglandins and thromboxane increased during the glomerular hyperfiltration response to a meat meal and was suppressed by aspirin administration which did not suppress the renal hemodynamic response to the meat meal. The data do not support a causal role for prostaglandins and thromboxane A2 in the hemodynamic response to acute protein loading.
The loop of Henle contributes to renal acidification by reabsorbing about 15% of filtered bicarbonate. To study the effects on loop of Henle bicarbonate transport (JHCO3) of acid-base disturbances and of several factors known to modulate sodium transport, these in vivo microperfusion studies were carried out in rats during: (a) acute and chronic metabolic acidosis, (b) acute and chronic (hypokalemic) metabolic alkalosis, (c) a control sodium diet, (d) a high-sodium diet, (e) angiotensin II (AII) intravenous infusion, (f) simultaneously intravenous infusion of both AII and the AT1 receptor antagonist DuP 753, (g) acute ipsilateral mechanicochemical renal denervation. Acute and chronic metabolic acidosis increased JHCO3; acute metabolic alkalosis significantly reduced JHCO3, whereas chronic hypokalemic alkalosis did not alter JHCO3. Bicarbonate transport increased in animals on a high-sodium intake and following AII administration, and the latter was inhibited by the AII (AT1) receptor antagonist DuP 753; acute renal denervation lowered bicarbonate transport. These data indicate that bicarbonate reabsorption along the loop of Henle in vivo is closely linked to systemic acid-base status and to several factors known to modulate sodium transport.
Twenty middle aged endurance runners underwent physiological testing to determine their maximal oxygen uptake (VO2max), lactate threshold, ventilatory threshold, the slope variation point (SVP) of the linear relationship between running speed (RS) and heart rate (HR) both on the treadmill and during a field test, and the onset of blood lactate accumulation point. The RS, HR, VO2 and blood lactate concentration at which the different thresholds occurred were highly correlated (0.70 < r < 0.95; p < 0.01). The various indices of aerobic-anaerobic transition in the master athletes examined were shown to occur at a comparable percentage of their VO2max as compared to their younger counterparts. The tests developed for, and commonly used in adult athletes, are equally valid in this age group.
The Keller-Lelievre technique for hallux valgus correction was modified by detaching the extensor hallucis brevis tendon from the proximal phalanx, and reattaching it on the medial sesamoid. Thirty-five consecutive patients were assigned randomly to 1 of 2 groups. Patients in Group 1 received the modified operation, and the original Keller-Lelievre technique was used for the control group. The only significant radiographic difference at 6 months was the distance between the first and the fifth metatarsal heads. There were only slightly significant differences in function and in pain relief between the 2 groups at the 6th postoperative month. At 3 years, these differences were greater, with the group treated by the modification described herein, retaining significant correction and showing better functional results.
Among other factors, articular cartilage degeneration is caused by proteolytic enzymes. Different cell types of the synovial fluid and/or the synovial membrane and cartilage release specific proteases. Normally, these are finely tuned with their inhibitors. When this balance is altered, the proteolytic action may prevail, producing tissue damage, cartilage disruption, and ultimately a full osteoarthritic picture. The protease antiprotease mechanism opens new perspectives in the diagnosis and pharmacologic management of osteoarthritis. Early diagnosis and improved monitoring of the evolution of the disease are made possible, and a more rational therapy against cartilage disruption becomes feasible.