Effects of Leg Length, Sex, Laterality, and the Intermediate Femoral Cutaneous Nerve on Infrapatellar Innervation.

Background: An iatrogenic injury to the infrapatellar branch of the saphenous nerve (IPBSN) is a common precipitant of postoperative knee pain and hypoesthesia. Purpose: To locate potential safe zones for incision by observing the patterns and pathway of the IPBSN while examining the relationship of its location to sex, laterality, and leg length. Study Design: Descriptive laboratory study. Methods: A total of 107 extended knees from 55 formalin-embalmed cadaveric specimens were dissected. The nerve was measured from palpable landmarks: the patella at the medial (point A) and lateral (point B) borders of the patellar ligament, the medial border of the patellar ligament at the patellar apex (point C) and tibial plateau (point D), the medial epicondyle (point E), and the anterior border of the medial collateral ligament at the tibial plateau (point F). The safe zone was defined as 2 SDs from the mean. Results: Findings indicated significant correlations between leg length and height (r P = 0.832; P < .001) as well as between leg length and vertical measurements (≥45°) from points A and B to the IPBSN (r P range, 0.193-0.285; P range, .004-.049). Male specimens had a more inferior maximum distance from point A to the intersection of the IPBSN and the medial border of the patellar ligament compared with female specimens (6.17 vs 5.28 cm, respectively; P = .049). Right knees had a more posterior IPBSN from point F compared with left knees (-0.98 vs-0.02 cm, respectively; P = .048). The majority of knees (62.6%; n = 67) had a nerve emerging that penetrated the sartorius muscle. Additionally, 32.7% (n = 35) had redundant innervation, and 25.2% (n = 27) had contribution from the intermediate femoral cutaneous nerve (IFCN). Conclusion: We identified no safe zone. Significant innervation redundancy with a substantial contribution to the infrapatellar area from the IFCN was noted and contributed to the expansion of the danger zone. Clinical Relevance: The location of incision and placement of arthroscopic ports might not be as crucial in postoperative pain management as an appreciation of the variance in infrapatellar innervation. The IFCN is a common contributor. Its damage could explain pain refractory to SN blocks and therefore influence anesthetic and analgesic decisions.

Five-Year Incidence, Management, and Visual Outcomes of Diffuse Lamellar Keratitis after Femtosecond-Assisted LASIK.

Femtosecond (FS) lasers initially had a higher incidence of diffuse lamellar keratitis (DLK) compared with microkeratome flap creation. It has been theorized that higher-frequency lower-energy (HFLE) FS lasers would reduce the incidence of DLK. Our study sought to evaluate the incidence of newer HFLE FS lasers with pulse frequencies above 60 kHz. It was a retrospective case-control study evaluating the incidence of DLK following flap creation with one of three FS lasers (AMO iFs, WaveLight FS200, Zeiss VisuMax). Uncomplicated LASIK cases were included as the control group (14,348 eyes) and cases of DLK were recorded in the study group (637 eyes). Of the 637 cases of DLK, 76 developed stage II, 25 progressed to stage III, and only three developed stage IV DLK. The overall incidence rate of DLK was 4.3%; it has fallen with the invention of newer HFLE FS lasers and is approaching the DLK incidence rates of DLK with microkeratome.

Neuropathic Corneal Pain Following LASIK Surgery: A Retrospective Case Series.

INTRODUCTION: Transient dry eye symptoms have been reported following laser in situ keratomileusis (LASIK). Very rarely, patients may present with debilitating symptoms of dry eye syndrome (DES) with limited or no evidence of ocular surface disease. These patients are diagnosed with a form of DES known as neuropathic corneal pain (NCP). PATIENTS AND METHODS: This study is a retrospective medical record review of a case series of 18 patients who developed NCP post-LASIK over the years 1996-2021. All patients who developed severe ocular pain following LASIK consistent with NCP were included. Patients with severe ocular pain who had evidence of severe ocular surface disease or other ophthalmic etiology to explain their debilitating symptoms were not included. RESULTS: The average age of patients in our study was 39.5 years. The majority of our patients were female (72.2%) and of Caucasian ancestry (83.3%). The average onset of symptoms was 9.6 months post-LASIK. Patients had past medical histories significant for neuropsychiatric conditions (50%), functional pain syndromes (22.2%), autoimmune diseases (33.3%), and hypothyroidism (27.8%), and the occurrence of these was higher than the national prevalence of these diseases. Symptoms were consistent with the severity and characteristics defining NCP. Treatment was multimodal, involved topical and systemic therapies, and was unique to each patient. Overall, the majority of patients had clinical improvement in symptoms following treatment with regular follow-up. CONCLUSION: Although rare, the 26-year prevalence of NCP post-LASIK in our study was roughly 1 in 900 cases. The mean time to onset after surgery was delayed at 9.6 months. Certain risk factors such as neuropsychiatric conditions, history of functional pain syndromes, history of autoimmune conditions, and hypothyroidism may predispose patients to the development of this condition. Patients benefited from proper diagnosis and a multimodal approach to treatment.

Anterior Chamber Retained Lens Fragments After Cataract Surgery: A Case Series and Narrative Review.

INTRODUCTION: Retained lens fragments in the anterior chamber following cataract extraction (CE) with phacoemulsification are rare but can lead to significant patient morbidity. Our study aimed to identify risk factors associated with retained lens fragments. METHODS: Patients who underwent cataract surgery and subsequently identified to have retained lens fragments in the anterior segment were included. Incidence per year, patient demographics, visual acuity, ocular biometrics, surgical technique, surgeon performing CE, and outcomes were collected retrospectively and compared to a control group. RESULTS: Twenty-four patients were identified with retained lens fragments, with an incidence of 0.10%. The mean age was 76 years ±6.72 (60-80) compared to 63 ±11.41 (22-86) in the control group (p <0.001). Patients with UDVA 20/150 or worse experienced a greater average improvement in visual acuity compared to patients with UDVA better than 20/150 (logMAR 0.46 vs logMAR 0.05). The mean intraocular pressures before (CE), after CE but before fragment removal, and following fragment removal were 14 mmHg ±2.59, 19 mmHg ±8.20, and 11 mmHg ±2.75, respectively. Twenty-two patients presented with inferiorly located fragments. Statistically significant biometrics include mean anterior chamber depth (3.1 mm ±0.37 vs 3.33 mm ±0.39, p = 0.01) and lens thickness (4.77 mm ±0.44 vs 4.35 mm ±0.44, p = <0.001). Yearly incidence rates per surgeon ranged from 0.00% to 0.85%. In 2003 and 2004, one surgeon had significantly higher incidence rates (0.31 and 0.40%) compared to the average combined rate of all surgeons throughout the study (0.10), with p values of 0.001 and 0.003, respectively. The mean number of days between CE and fragment removal was 26 ±40 (1-138). CONCLUSION: Increased patient age, shallow anterior chamber depth, and thick lens may be risk factors for retained lens fragments. There may be additional surgeon-specific risk factors. Phacoemulsification technique (Divide-and-Conquer versus Horizontal Chop) showed no significant difference.

Inhibition of the receptor for advanced glycation end-products (RAGE) protects from secondhand smoke (SHS)-induced intrauterine growth restriction IUGR in mice.

Intrauterine growth restriction (IUGR) is a disease affecting 10% of all pregnancies. IUGR is associated with maternal, fetal, or placental abnormalities. Studies investigating the effects of secondhand smoke (SHS) exposure and IUGR are limited. The receptor for advanced glycation end-products (RAGE) is a pro-inflammatory transmembrane receptor increased by SHS in the placenta. We tested the hypothesis that inhibition of RAGE during SHS exposure protects from smoke-induced IUGR. C57BL/6 mice were exposed to SHS or SHS + semi-synthetic glycosaminoglycan ethers (SAGEs) known to inhibit RAGE signaling. Trophoblast cells were treated with cigarette smoke extract (CSE) with or without SAGEs in order to address the effects of RAGE inhibition during trophoblast invasion in vitro. SHS-treated mice demonstrated a significant reduction in fetal weight (7.35-fold, P ≤ 0.0001) and placental weight (1.13-fold, P ≤ 0.0001) compared with controls. Mice co-treated with SHS and SAGEs were protected from SHS-induced fetal weights decreases. SHS treatment of C57BL/6 mice activated placental extracellular signal-regulated kinase (ERK) (3.0-fold, P ≤ 0.05), JNK (2.4-fold, P ≤ 0.05) and p38 (2.1-fold, P ≤ 0.05) and the expression of inflammatory mediators including TNF-α (1.34-fold, P ≤ 0.05) and IL-1ß (1.03-fold, P ≤ 0.05). SHS-mediated activation of these molecules was reduced to basal levels when SAGE was co-administered. Invasion of trophoblast cells decreased 92% (P < 0.002) when treated with CSE and CSE-mediated invasion was completely reversed by SAGEs. We conclude that RAGE inhibition protects against fetal weight loss during SHS-induced IUGR. These studies provide insight into tobacco-mediated IUGR development and clarify avenues that may be helpful in the alleviation of placental complications.

Cigarette smoke and decreased oxygen tension inhibit pulmonary claudin-6 expression.

PURPOSE: Chronic obstructive pulmonary disease is a condition involving perturbed barrier integrity coincident with both emphysema and inflammation of the airways, and smoking is considered a major risk factor. Claudins (Cldns) stabilize barriers and contribute to tight junctions by preventing paracellular transport of extracellular fluid constituents. METHODS: To determine Cldn6 was differentially influenced by tobacco smoke, Cldn6 was evaluated in cells and tissues by q-PCR, immunoblotting, and immunohistochemistry following exposure. Cldn6 transcriptional regulation was also assessed using luciferase reporter constructs. RESULTS: Q-PCR and immunoblotting revealed that Cldn6 was decreased in alveolar type II-like epithelial cells (A549) and primary small airway epithelial cells when exposed to cigarette smoke extract (CSE). Cldn6 was also markedly decreased in the lungs of mice exposed to acute tobacco smoke delivered by a nose-only automated smoke machine compared to controls. Luciferase reporter assays incorporating 0.5-kb, 1.0-kb, or 2.0-kb of the Cldn6 promoter revealed decreased transcription of Cldn6 following exposure to CSE. Cldn6 transcriptional regulation was also assessed in hypoxic conditions due to low oxygen tension observed during smoking. Hypoxia and hypoxia inducible factor-1 alpha caused decreased transcription of the Cldn6 gene via interactions with putative response elements in the proximal promoter sequence. CONCLUSIONS: These data reveal that tight junctional proteins such as Cldn6 are differentially regulated by tobacco-smoke exposure and that Cldns are potentially targeted when epithelial cells respond to tobacco smoke. Further research may show that Cldns expressed in tight junctions between parenchymal cells contribute to impaired structural integrity of the lung coincident with smoking.

Up-Regulation of Claudin-6 in the Distal Lung Impacts Secondhand Smoke-Induced Inflammation.

It has long been understood that increased epithelial permeability contributes to inflammation observed in many respiratory diseases. Recently, evidence has revealed that environmental exposure to noxious material such as cigarette smoke reduces tight junction barrier integrity, thus enhancing inflammatory conditions. Claudin-6 (Cldn6) is a tetraspanin transmembrane protein found within the tight junctional complex and is implicated in maintaining lung epithelial barriers. To test the hypothesis that increased Cldn6 ameliorates inflammation at the respiratory barrier, we utilized the Tet-On inducible transgenic system to conditionally over-express Clnd6 in the distal lung. Cldn6 transgenic (TG) and control mice were continuously provided doxycycline from postnatal day (PN) 30 until euthanasia date at PN90. A subset of Cldn6 TG and control mice were also subjected to daily secondhand tobacco smoke (SHS) via a nose only inhalation system from PN30-90 and compared to room air (RA) controls. Animals were euthanized on PN90 and lungs were harvested for histological and molecular characterization. Bronchoalveolar lavage fluid (BALF) was procured for the assessment of inflammatory cells and molecules. Quantitative RT-PCR and immunoblotting revealed increased Cldn6 expression in TG vs. control animals and SHS decreased Cldn6 expression regardless of genetic up-regulation. Histological evaluations revealed no adverse pulmonary remodeling via Hematoxylin and Eosin (H&E) staining or any qualitative alterations in the abundance of type II pneumocytes or proximal non-ciliated epithelial cells via staining for cell specific propeptide of Surfactant Protein-C (proSP-C) or Club Cell Secretory Protein (CCSP), respectively. Immunoblotting and qRT-PCR confirmed the differential expression of Cldn6 and the pro-inflammatory cytokines TNF-α and IL-1ß. As a general theme, inflammation induced by SHS exposure was influenced by the availability of Cldn6. These data reveal captivating information suggesting a role for Cldn6 in lungs exposed to tobacco smoke. Further research is critically necessary in order to fully explain roles for tight junctional components such as Cldn6 and other related molecules in lungs coping with exposure.

Determinants of Club Head Speed in PGA Professional Golfers.

Turner, AN. Determinants of club head speed in PGA professional golfers. J Strength Cond Res 30(8): 2266-2270, 2016-Club head speed (CHS) has been significantly correlated with golf performance, but only in amateurs. The purpose of this study therefore, was to investigate the relationship between field-based measures of strength and power with CHS in Professional Golfers Association (PGA) professional golfers, and further determine differences between age groups. A correlation design was used to test relationships between squat jump (SJ), seated medicine ball throw (SMBT), rotational medicine ball throw (RMBT), and CHS. Twenty participants volunteered to take part in the study (age, 31.95 ± 8.7 years; height, 182.75 ± 6.88 cm; mass, 90.47 ± 15.6 kg). Intraclass correlation coefficients reported high reliability for performance variables (r = 0.85-0.95). Significant correlations (p < 0.01) were found between CHS and SJ (r = 0.817) and SMBT (r = 0.706), but not RMBT (r = 0.572). A stepwise linear regression analysis identified that SJ and SMBT explained 74% of the variance in CHS. When dividing the sample based on age, professionals <30 years (n = 10; 25.6 ± 2.9 years) displayed significantly (p ≤ 0.05) higher CHS and SJ height compared with professionals >30 (n = 10; 39.7 ± 5.5 years). Correlations to CHS for <30 were significant for SJ (r = 0.801) and SMBT (r = 0.643), but nonsignificant for RMBT. Those >30 had significant correlations to CHS not only in SMBT (r = 0.881) and SJ (r = 0.729), but also in RMBT (r = 0.642). The results of this study suggest that SJ and SMBT have the largest contribution to CHS in PGA professional golfers. When comparing age groups, it appears that younger golfers (<30 years) utilize more leg strength whereas older golfers (>30 years) utilize more upper body strength. Results suggest that strength-based leg exercises and power-based chest exercises may improve CHS in professional golfers.