Dural defect repair with fascia by a CO2 laser system in a porcine model

HYPOTHESIS/OBJECTIVES: We tested the effectiveness of a temperature-controlled CO2 laser soldering system on a porcine model for dural defect reconstruction using a fascial patch. METHODS: A dural patch was excised and then reconstructed with fascia by a CO2 laser system in vitro in 27 animals and in vivo in five animals. RESULTS: After dural reconstruction, the average burst pressure of the soldered patch in vitro, as measured by a custom-made pressure detector, was 258.5 cm H2O. All five pigs in the in vivo group showed no neurological complications or cerebrospinal fluid leak, and the underlying brain tissue showed no thermal injury. CONCLUSION: The CO2 laser system created a watertight bond and did not cause thermal injury to the brain. The procedure is potentially faster than conventional repair, and wound healing may also be more rapid.     

The changing epidemiology of leptospirosis in Israel.

We reviewed all serologically confirmed cases of leptospirosis from 1985 to 1999 in Israel, where the disease is endemic. There were 59 cases, with an average annual incidence of 0.05/100,000. The dominant serogroup, Leptospira icterohemorrhagica, occurred in 29% of patients; in an earlier study (1970-1979), it accounted for only 2%. Serogroups that occurred mainly in rural areas accounted previously for 79% but had declined to 32%.     

Two distinct non-T helper type 2 interleukin-4 cell subsets in mice as revealed by single-cell cytokine analysis

We have previously defined four murine CD4⁺ peripheral T cell subsets, fractions (Fr.) I – IV, based on expression of the 6C10 and 3G11 determinants (Hayakawa, K. and Hardy, R. R., J. Exp. Med. 1988. 168: 1825). These subsets also show distinctive levels of other cell surface markers: the two minor subsets, Fr. III and Fr. IV, are both CD45RB^low/-, L-selectin (Mel-14)^? and CD44^hi, characteristic of secondary T cells. The patterns and levels of cytokine production by individual cells in each subset were determined by bioassay for interleukin (IL)-2/IL-4 or IL-4/interferon (IFN)-γ production after anti-CD3 stimulation. Our data revealed that these four phenotypically defined subsets largely coincide with clusters of cells showing uniform distinctive cytokine profiles, i.e. IL-2⁺/IFN-γ^?/IL-4^? (Fr. I and Fr. II, L-selectin⁺), IL-2⁺/IFN-γ⁺/IL-4⁺ (Fr. III, L-selectin^?), and IL-2^?/IFN-γ^low/-/IL-4⁺ (Fr. IV, L-selectin^?). Besides these subsets, an L-selectin-negative cell subfraction within Fr. II appears to represent a transitional population between the IL-2⁺/IFN-γ^?/IL-4^? stage and the IL-2⁺/IFN-γ⁺/IL-4⁺ stage. Taken together, these results demonstrate the presence of two IL-4⁺ secondary T cell subsets with distinct cytokine production patterns, and show that the majority of IL-4⁺ cells found in healthy adult laboratory mice co-produce IFN-γ, and thus are not typical T helper type 2 cells.     

Changes in renal prostanoid synthesis induced by potassium loading in rats

Previous works have demonstrated changes in the urinary excretion of prostaglandins (PG) in response to changes in potassium (K) or sodium (Na) intake. In the present study, the production of PGE2, PGF2 alpha, 6-keto-PGF1 alpha and thromboxane B2 (TXB2) by isolated glomeruli, cortical homogenates, medullary and papillary slices was measured in K-loaded rats on either a normal or a low Na intake. In glomeruli, K loading increased selectively PGE2 synthesis. In Na-depleted animals, all prostanoids were elevated and K loading did not induce a further increase. In cortical and medullary preparations, PGE2 was decreased by K loading irrespective of the state of Na balance. In papilla, PGE2 decreased (in all K-loaded rats) and PGF2 alpha increased (only in rats with normal Na intake). 6-Keto-PGF1 alpha and TXB2 did not change significantly. No correlation was present between changes of PG synthesis and urinary kallikrein excretion. The results demonstrate a specific effect of K on PGE2 and PGF2 alpha, and suggest a role for these substances in K homeOstasis.     

Penetrating keratoplasty in rabbits with herpetic keratitis treated with poly I:C

Penetrating keratoplasties were performed in which grafts were exchanged between normal rabbits and rabbits previously infected with Herpes simplex virus (HSV). Clear grafts were obtained when surgery was performed during the latent stage of the disease (3 months after HSV inoculation). Polyinosinic acid: polycytidylic acid (poly I:C) was administered before and after keratoplasty when the rabbits had active herpetic keratitis. Clear grafts were obtained when the rabbits were inoculated with HSV and treated 18 hours later with poly I:C, which was continued until two weeks before keratoplasty. This treated group had a rapid decrease in HSV titer, inhibition of the migration of HSV from the infected cornea to the trigeminal ganglia, and a decrease in antibody titer to HSV in the sera. In rabbits inoculated with HSV, subjected two weeks later to keratoplasty, and then treated with poly I:C, three quarters of the graft rejections were milder than those in the control group.     

NADH-dependent prostaglandin E2-9-ketoreductase activity and prostaglandin synthesis in the Brattleboro rat kidney: effects of the antidiuretic hormone

The activity of prostaglandin (PG)E2-9-ketoreductase (9KR), an enzyme catalyzing the conversion of PGE2 to PGF2 alpha, was significantly increased in glomerular and cortical homogenates of diabetes insipidus (DI) rats, as compared to normal Long Evans (LE) rats, and did not change with ADH treatment. Medullary 9KR was similar in the three groups and papillary 9KR was increased, but not significantly, in both groups of DI rats. Km values for PGE2 and NADH were compared in the various compartments of the kidney. Levels of 9KR were not correlated with the PGE/PGF ratio in urine or supernatants. The synthesis of PGE2 and PGF2 alpha by isolated glomeruli was increased in DI rats. This was not reversed by ADH treatment, PGE2 synthesis increasing even further, especially in the presence of arachidonic acid. In contrast, medullary slices produced significantly less PGs in DI than in LE rats and returned to normal with ADH treatment. Papillary slices produced similar quantities of prostaglandins in all groups. The results do not support the concept that the alterations in PG synthesis observed in DI rat are related only to changes in 9KR activity, but do not exclude the possibility that the enzyme participates in the regulation of PG biosynthesis.     

Painful entrapment of the lateral antebrachial cutaneous nerve at the elbow

PURPOSE: The purpose of this study was to report the diagnosis and management of entrapment neuropathy of the lateral antebrachial cutaneous nerve (LABCN) presenting as lateral elbow pain. METHODS: Twenty-three patients with lateral elbow pain were diagnosed with entrapment of the LABCN. Six patients also had paresthesia of the distal forearm. Diagnosis was made by clinical evaluation and confirmed with diagnostic injection of 1% lidocaine. Electrodiagnostic evaluation was positive in all patients. All patients were treated conservatively. Seven patients improved and 16 patients had surgical decompression of the LABCN at the elbow and distal arm with partial resection of the lateral margin of the biceps tendon. Postoperative follow-up evaluation averaged 45 months. RESULTS: Fourteen patients had complete relief of pain and 2 patients continued to have minimal to mild pain. Of the 6 patients who had preoperative paresthesia only 1 patient had persistent mild paresthesia of the radial side of the distal forearm. Range of motion and grip and pinch strength returned to normal values. All patients returned to their preoperative daily and work activities. CONCLUSIONS: Entrapment neuropathy of the LABCN should be considered in the differential diagnosis of elbow pain. Electrodiagnostic evaluation can be very useful in establishing and confirming the diagnosis. Surgical treatment of patients who do not respond to conservative treatment is simple yet effective in improving the patients' symptoms. Patients who present with paresthesia usually require surgical intervention because paresthesia represents a more progressive stage of the nerve entrapment.     

Familial cardiomyopathy A review of 11 families

Findings in 11 families with cardiomyopathy are reviewed. Of 98 persons examined, 47 were affected. Their mean age at the time of detection was 24 years (range 2 to 61 years). The diagnosis was made by exclusion. The presence of other affected members, often in 2 or 3 generations of the same family, enabled us to establish the familial character.

The clinical findings included palpitations, arrhythmias, syncope and sudden death. Nine patients had intractable congestive heart failure, and 6 Stokes-Adams attacks; 4 of the 6 had implanted pacemakers. Several patients had proved or suspected hypertrophic subaortic stenosis.

The electrocardiogram proved to be the best single tool for the detection of cardiomyopathy. Rhythm disturbances, left ventricular hypertrophy, intraventricular conduction defects and abnormal Q waves were frequent. The Wolff-Parkinson-White pattern was found in 4 patients. Clinically the diagnosis of mitral valve disease and myocardial infarction was often considered.

The prognosis is uncertain; when first detected 28 patients were asymptomatic, and only 13 have remained asymptomatic during a follow-up period of 7 years. Ten of the 47 patients died during this period, and in the 9 who came to autopsy, no congenital, rheumatic, infectious or coronary heart disease was found. The hearts were enlarged, and histologie examination revealed diffuse fibrosis with severe hypertrophy of the muscle fibers.

Of special interest were the dynamic changes in the electrocardiogram with the disappearance of the abnormal Q waves and infarctionlike patterns with advancing age, as well as appearance of left bundle branch block. Serum enzyme disturbances were detected in some families, and their possible significance is discussed.

Genetically, the findings are consistent with transmission by an autosomal dominant gene with high penetrance.     

Secondary Prevention of Colorectal Adenomas: Is There an Optimal Follow-up for Colorectal Adenomas?

Colorectal cancer is the second most common cause of cancer-related death in the Western world. Its development is typically through colorectal adenomas. Colorectal cancer prevalence may be reduced substantially by primary prevention including colonoscopy and polypectomy. Secondary prevention applies to populations that have been diagnosed with colorectal adenomas, and its goal is to prevent the development of additional adenomas. It is accomplished mainly by endoscopic surveillance with polypectomy. Additional measures include chemoprevention, used in selected patients only, and modification of risk factors such as smoking, high body mass index, and poor nutrition. This article reviews the current professional guidelines for endoscopic surveillance and adherence by physicians and patients. Measures to increase surveillance efficacy include standardization of colonoscopy among endoscopists and enhanced endoscopy techniques. This article also reviews evidence for the impact of lifestyle modification. It appears that the endoscopic surveillance protocol is often personalized because of the lack of standardization of baseline colonoscopy, suboptimal adherence to the guidelines, and a deficiency in the guidelines with regard to proper risk stratification.     

Thyroid Dysfunction in Patients Treated With Sunitinib or Sorafenib

IntroductionSunitinib and sorafenib are tyrosine kinase inhibitors used in metastatic renal cell carcinoma and are known to cause hypothyroidism in a subset of patients. The goal of this study was to better characterize the development of hypothyroidism in patients and to examine its relationship to progression-free survival.Patients and MethodsA retrospective chart review was performed on patients treated with sunitinib or sorafenib from January 1, 2005, to January 1, 2011. Data pertaining to the treatment course and development of hypothyroidism were extracted. Patients with hypothyroidism at the beginning of treatment were analyzed separately.ResultsA total of 73 treatment periods had sufficient data to analyze. Among patients with normal baseline thyroid function, 15 (44%) of 34 patients treated with sunitinib and 6 (27%) of 22 patients treated with sorafenib developed hypothyroidism. The hazard ratio for the development of hypothyroidism with sorafenib vs. sunitinib treatment was significant, at 0.38 (95% CI, 0.14-0.97). There was a statistically significant difference in the progression-free survival between patients who developed hypothyroidism while receiving treatment compared with those who did not, 18.2 vs. 10.1 months (P = .01).ConclusionsThis study demonstrated a significant difference in the incidence of hypothyroidism during treatment with sunitinib and sorafenib, with a higher incidence of hypothyroidism in patients treated with sunitinib. The development of hypothyroidism was associated with a longer progression-free survival.